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HbAc role in insulin resistance

HbAc role in insulin resistance

Cardiovasc Diabetol resishance Article Google Scholar Immune-boosting foods S, Menstrual health experts RR, Miller WG, Resistancf M, Myers G, Caudill HbAcc, Campbell SE, Steffes Resstance Standardization of insulin immunoassays: report of the American Diabetes Association workgroup. Regulation of and intervention into the oxidative pentose phosphate pathway and adenine nucleotide metabolism in the heart. Search in Google Scholar If you do, there are a lot of lifestyle factors that can help reduce or reverse it. Article CAS Google Scholar. Get Permissions. Annu Rev Physiol.

HbAc role in insulin resistance -

Glycated hemoglobin HbA1c has been considered as a potentially good indicator of overall glycemic exposure and likely risk for long-term complications. Therefore, this study is designed to investigate the importance of HbA1c in predicting insulin resistance among apparently healthy at-risk German populations.

Moreover, the ROC curve also showed that the HbA1c occupied a significant area under the curve 0. This is a preview of subscription content, log in via an institution to check access. Rent this article via DeepDyve.

Institutional subscriptions. American Diabetes Association Diagnosis and classification of diabetes mellitus. Diabetes Care 30 suppl 1 :S42—S Article Google Scholar. Diabetes Care 33 suppl 1 :S62—S Article PubMed Central Google Scholar.

Bergman RN, Phillips LS, Cobelli C Physiologic evaluation of factors controlling glucose tolerance in man: measurement of insulin sensitivity and beta-cell glucose sensitivity from the response to intravenous glucose. J Clin Invest — Article CAS PubMed PubMed Central Google Scholar.

Bonora E, Calcaterra F, Lombardi S, Bonfante N, Formentini G, Bonadonna RC, Muggeo M Plasma glucose levels throughout the day and HbA 1c interrelationships in type 2 diabetes: implications for treatment and monitoring of metabolic control.

Diabetes Care — Article CAS PubMed Google Scholar. Brehm A, Pfeiler G, Pacini G, Vierhapper H, Roden M Relationship between serumlipoprotein ratios and insulin resistance in obesity. Clin Chem — Carson AP, Reynolds K, Fonseca VA, Muntner P Comparison of A1C and fasting glucose criteria to diagnose diabetes among US adults.

Cavaghan MK, Ehrmann DA, Polonsky KS Interactions between insulin resistance and insulin secretion in the development of glucose intolerance. DeFronzo RA Lilly lecture. The triumvirate: beta-cell, muscle, liver. A collusion responsible for NIDDM.

Diabetes — DeFronzo RA, Tobin JD, Andres R Glucose clamp technique: a method for quantifying insulin secretion and resistance. Am J Physiol E—E CAS PubMed Google Scholar. Ferrannini E, Buzzigoli G, Bonadonna R, Giorico MA, Oleggini M, Graziadei L, Pedrinelli R, Brandi L, Bevilacqua S Insulin resistance in essential hypertension.

N Engl J Med — Ferrara CM, Goldberg AP Limited value of the homeostasis model assessment to predict insulin resistance in older men with impaired glucose tolerance. Grundy SM Pre-diabetes, metabolic syndrome, and cardiovascular risk. J Am Coll Cardiol — Gulli G, Ferrannini E, Stern M, Haffner S, DeFronzo RA The metabolic profile of NIDDM is fully established in glucose-tolerant offspring of two Mexican-American NIDDM parents.

Herman WH, Ma Y, Uwaifo G, Haffner S, Kahn SE, Horton ES, Lachin JM, Montez MG, Brenneman T, Barrett-Connor E, Diabetes Prevention Program Research G Differences in A1C by race and ethnicity among patients with impaired glucose tolerance in the diabetes prevention program.

Hosker JP, Matthews DR, Rudenski AS, Burnett MA, Darling P, Bown EG, Turner RC Continuous infusion of glucose with model assessment: measurement of insulin resistance and beta-cell function in man.

Diabetologia — International Expert Committee International Expert committee report on the role of the A1C assay in the diagnosis of diabetes. Jeon JY, Ko SH, Kwon HS, Kim NH, Kim JH, Kim CS, Song KH, Won JC, Lim S, Choi SH, Jang MJ, Kim Y, Oh K, Kim DJ, Cha BY, Taskforce Team of Diabetes Fact Sheet of the Korean Diabetes A Prevalence of diabetes and prediabetes according to fasting plasma glucose and HbA1c.

Karhapaa P, Voutilainen E, Kovanen PT, Laakso M Insulin resistance in familial and nonfamilial hypercholesterolemia. Arterioscleresis and Thrombosis — Article CAS Google Scholar. Klein R, Klein BE, Moss SE, Davis MD, DeMets DL Glycosylated hemoglobin predicts the incidence and progression of diabetic retinopathy.

J Am Med Assoc — Laakso M, Pyorala K, Voutilainen E, Marniemi J Plasma insulin and serum lipids and lipoproteins in middle-aged non- insulin dependent diabetic and non-diabetic subjects. Am J Epidemiol — Lee JM, Okumura MJ, Davis MM, Herman WH, Gurney JG Prevalence and determinants of insulin resistance among US adolescents: a population based study.

Article PubMed Google Scholar. Cardiovasc Diabetol —9. Marcovina S, Bowsher RR, Miller WG, Staten M, Myers G, Caudill SP, Campbell SE, Steffes MW Standardization of insulin immunoassays: report of the American Diabetes Association workgroup.

Matsuda M, DeFronzo RA Insulin sensitivity indices obtained from oral glucose tolerance testing. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man.

McLaughlin T, Abbasi F, Cheal K, Chu J, Lamendola C, Reaven GM Use of metabolic markers to identify overweight individuals who are insulin resistant. Ann Intern Med — McLaughlin T, Reaven GM, Abbasi F, Lamendola C, Saad M, Waters D, Simon J, Krauss RM Is there a simple way to identify insulin resistant individuals at increased risk of cardiovascular disease?

Am J Cardiol — Moran A, Jacobs DR, Steinberger J, Hong CP, Prineas R, Luepker R, Sinaiko AR Insulin resistance during puberty: results from clamp studies in children.

Moro E, Gallina P, Pais M, Cazzolato G, Alessandrini P, Bittolo-Bon Govindarajalu S Hypertriglyceridemia is associated with increased insulin resistance in subjects with normal glucose tolerance: evaluation in a large cohort of subjects assessed with the World Health Organization criteria for the classification of diabetes.

Metabolism — Perkovic V, Verdon C, Ninomiya T, Barzi F, Cass A, Patel A, Jardine M, Gallagher M, Turnbull F, Chalmers J, Craig J, Huxley R The relationship between proteinuria and coronary risk: a systematic review and meta-analysis.

PLoS Med 5:e Article PubMed PubMed Central Google Scholar. Reaven GM Role of insulin resistance in human disease. Satchell SC, Tooke JE What is the mechanism of microalbuminuria in diabetes: a role for the glomerular endothelium?

Simental-Mendia LE, Rodriguez-Moran M, Guerrero-Romero F The product of fasting glucose and triglycerides as surrogate for identifying insulin resistance in apparently healthy subjects.

Metab Syndr Relat Disord — Tapp RJ, Shaw JE, Zimmet PZ, Balkau B, Chadban SJ, Tonkin AM, Welborn TA, Atkins RC Albuminuria is evident in the early stages of diabetes onset: results from the Australian diabetes, obesity, and lifestyle study AusDiab.

American Journal of Kidney Diseases. The official journal of the National Kidney Foundation — Tuomilehto J, Lindstrom J, Eriksson JG, Valle TT, Hamalainen H, Ilanne-Parikka P, Keinanen-Kiukaanniemi S, Laakso M, Louheranta A, Rastas M, Salminen V, Uusitupa M, Finnish Diabetes Prevention Study G: Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance.

The New England Journal of Medicine; — Yeni-Komshian H, Carantoni M, Abbasi F, Reaven GM Relationship between several surrogate estimates of insulin resistance and quantification of insulin-mediated glucose disposal in healthy nondiabetic volunteers.

Ziemer DC, Kolm P, Weintraub WS, Vaccarino V, Rhee MK, Twombly JG, Narayan KM, Koch DD, Phillips LS Glucose-independent, black-white differences in hemoglobin A1c levels: a cross-sectional analysis of 2 studies. Download references.

HbA 1c analysis was performed by affinity chromatography HPLC on Primus Ultra2 Analyzer Primus Corporation, Kansas City, Kansas, USA.

Statistical analyses were conducted using the statistical package SPSS version 17 SPSS Inc. Independent samples t-test and χ 2 test were used for comparison of insulin resistant and insulin sensitive groups. Multivariate linear regression analysis was used for determining the association between HbA 1c and independent variables.

Variables with non-normal distribution were log transformed. A total of non-diabetic subjects were included in the study. There were individuals with normal glucose tolerance and individuals with pre-diabetes impaired fasting glucose, impaired glucose tolerance, or both according to ADA criteria.

Table 1 shows the characteristics of the study population. IFG, Impaired fasting glucose; IGT, impaired glucose tolerance. HbA 1c and other biochemical parameters of insulin resistant and insulin sensitive subjects were compared. Independent samples t-test used for comparisons unless otherwise indicated.

a p-Value determined using χ 2 test. To estimate the independent relationship between HbA 1c and HOMA-IR, multiple linear regression analysis was used.

Age, gender, fasting glucose, 2-h glucose and HOMA-IR were entered in the regression model as independent variables. Since HOMA-IR values had skewed distribution, log transformed HOMA-IR was used in analysis. Regression analysis showed that age, fasting glucose, 2-h glucose, and log transformed HOMA-IR values are significant predictors of HbA 1c.

Higher HOMA-IR values are associated with higher HbA 1c levels in non-diabetic subjects. Standardized β coefficients demonstrate the relative importance of predictor variables in regression model.

In the regression model age showed the highest standardized β coefficient. In non-diabetic subjects age was the most important factor affecting HbA 1c values Table 3.

HbA 1c values were also presented in different age groups Table 4. Dividing the study population as normal and pre-diabetic subjects and re-performing the regression analysis did not change the results fundamentally. Age was still most effective factor in predicting HbA 1c values in both normal group and pre-diabetic group.

Log HOMA was still a significant variable data not shown. To visualize the data a regression plot showing the relation between HbA 1c and HOMA-IR was generated. Scatterplot showing correlation between HOMA-IR and HbA 1c in different sample groups.

It was clearly reported that lower HbA 1c values were associated with reduced microvascular and macrovascular complications in diabetic patients [ 9 ].

Recently ADA recommended using HbA 1c also for the diabetes diagnosis and consolidated its importance in diabetes mellitus. The use of HbA 1c as a diagnostic criterion necessitates a more accurate measurement and careful interpretation.

Several factors other than plasma glucose levels were reported to affect glycated hemoglobin levels. Any condition affecting turnover of red blood cells like hemolytic anemia and iron deficiency affect HbA 1c levels.

Previous studies showed that genetic-ethnic factors, sex hormones and age are associated with HbA 1c values [ 10 ], [ 11 ], [ 12 ], [ 13 ], [ 14 ].

In the present study we report that HOMA-IR is a factor affecting HbA 1c values independent of fasting and 2-h post-load glucose concentrations. The relationship between glycated hemoglobin levels and glucose levels are higher in diabetic patients than in non-diabetic patients therefore it can be concluded that non-glycemic factors affecting HbA 1c levels are more important in non-diabetic patients [ 15 ].

Previous studies investigated the relationship between insulin resistance and HbA 1c. Gallwitz et al. showed that with increasing HbA 1c levels, there was a statistically significant increase in HOMA-IR in patients with type 2 DM [ 16 ].

Heianza et al. In another study Borai et al. showed that the correlation between HbA 1c and insulin resistance were higher in subjects with normal glucose tolerance than in patients with pre-diabetes and diabetes [ 18 ]. None of the aforementioned studies reported corrected results independent of glycemic status.

Venkataraman et al. showed that in a multivariate regression model with HbA 1c as dependent variable HOMA-IR log were significantly associated with HbA 1c independent of fasting glucose but the effect of post-load glucose on HbA 1c was lacking [ 19 ].

One recent study indicated that HbA 1c was associated with HOMA-IR independent of 0- and min glucose in pregnant women with gestational diabetes mellitus [ 20 ]. The results of our study reveal that HbA 1c is associated with HOMA-IR independent of fasting and post-load glucose status also in non-diabetic subjects.

Glycation is the nonenzymatic attachment of free aldehyde groups of carbohydrates to the unprotonated free amino groups of proteins [ 21 ]. The binding of glucose molecules to potential glycation sites in hemoglobin molecule leads to formation of HbA 1c. Via condensation with glucose, hemoglobin A first forms a labile intermediate adduct, which is thereafter rearranged to the more stable ketoamine adduct HbA 1c form [ 22 ].

Physiological factors like pH, inorganic phosphate, oxidative stress, deglycation, and Schiff base inhibitors can affect the rate of HbA 1c formation [ 23 ], [ 24 ], [ 25 ], [ 26 ], [ 27 ]. Another point to be considered is that glycation of hemoglobin occurs in the intracellular compartment. Previously, it was demonstrated that the erythrocyte glucose—to—plasma glucose concentration ratio may affect hemoglobin glycation and contributes to the variation in HbA 1c levels [ 28 ].

Oxidative stress is a process that was proposed to be associated with the multifactorial etiology of insulin resistance.

It was shown that plasma markers of oxidative stress were correlated with the degree of insulin resistance [ 29 ], [ 30 ]. Oxidative stress which is a factor co-existing with insulin resistance may also be responsible for the increased hemoglobin glycation.

Oxidative stress biomarkers as lipid peroxides were reported to be associated with hemoglobin glycation [ 31 ], [ 32 ]. LDL oxidation was also suggested to increase HbA 1c values [ 33 ]. Furthermore there is evidence that antioxidants can partially inhibit the formation of HbA 1c [ 31 ].

Consistent with previous studies, age was a significant factor affecting HbA 1c levels independent of glycaemia [ 13 ], [ 34 ]. However the mechanisms involved in the age related HbA 1c increase remain to be established. Since our model showed that age was the most effective factor contributing to the variation of HbA 1c levels in non-diabetic subjects it should not be ignored when interpreting an HbA 1c result.

The question whether age-specific diagnostic and treatment criteria would be appropriate was previously mentioned [ 13 ]. Due to its retrospective design the current study has some limitations.

Firstly the information of some possible confounding variables e. BMI could not be gathered; therefore confounding factors may exist. Second, HOMA-IR is not the gold standard method for measuring insulin sensitivity.

The euglycemic hyperinsulinemic clamp technique is the gold standard for quantifying insulin sensitivity; however, this technique requires insulin infusion and repeated blood sampling. HOMA-IR is a relatively simple method to determine insulin sensitivity.

It can be calculated from a single blood sample and it was reported to have a linear correlation with glucose clamp technique [ 35 ]. In conclusion, our data showed that HOMA-IR is associated with glycated hemoglobin values independent of glycaemia and age is a very important factor affecting HbA 1c values in non-diabetic subjects.

Conflict of interest: All authors declare that there is no conflict of interest regarding the publication of this article. Reaven GM. Pathophysiology of insulin resistance in human disease.

Physiol Rev ;— DeFronzo RA, Ferrannini E. Insulin resistance: a multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease.

Diabetes Care ;— Eckel RH, Grundy SM, Zimmet PZ. The metabolic syndrome. Lancet ;— Lillioja S, Mott DM, Howard BV, Bennett PH, Yki-Jarvinen H, Freymond D, et al. Impaired glucose tolerance as a disorder of insulin action.

Longitudinal and cross-sectional studies in Pima Indians. N Engl J Med ;— Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man.

Diabetologia ;—9. Saudek CD, Herman WH, Sacks DB, Bergenstal RM, Edelman D, Davidson MB. A new look at screening and diagnosing diabetes mellitus. J Clin Endocrinol Metab ;— International Expert Committee.

International Expert Committee report on the role of the A 1c assay in the diagnosis of diabetes. American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care ;—9. Stratton IM, Adler AI, Neil HA, Matthews DR, Manley SE, Cull CA, et al. Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes UKPDS 35 : prospective observational study.

BMJ ;— Herman WH, Ma Y, Uwaifo G, Haffner S, Kahn SE, Horton ES, et al. Diabetes prevention program research group. Differences in A 1c by race and ethnicity among patients with impaired glucose tolerance in the diabetes prevention program.

Diabetes Care ;—7. Cohen RM, Snieder H, LindsellCJ, Beyan H, Hawa MI, Blinko S, et al. Evidence for independent heritability of the glycation gap glycosylation gap fraction of HbA 1c in nondiabetic twins.

Snieder H, Sawtell PA, Ross L, Walker J, Spector TD, Leslie RD. HbA 1c levels are genetically determined even in type 1 diabetes: evidence from healthy and diabetic twins. Diabetes ;— Pani LN, Korenda L, Meigs JB, Driver C, Chamany S, Fox CS, et al. Effect of aging on A1c levels in individuals without diabetes: evidence from the Framingham Offspring Study and the National Health and Nutrition Examination Survey — Diabetes Care ;—6.

Page-Wilson G, Goulart AC, Rexrode KM. Interrelation between sex hormones and plasma sex hormone-binding globulin and Hemoglobin A1c in healthy postmenopausal women. Metab Syndr Relat Disord ;— Relationship between A1C and glucose levels in the general Dutch population: the new Hoorn study.

Diabetes Care;—6. Gallwitz B, Kazda C, Kraus P, Nicolay C, Schernthaner G. Contribution of insulin deficiency and insulin resistance to the development of type 2 diabetes: nature of early stage diabetes.

Acta Diabetol ;— Heianza Y, Arase Y, Fujihara K, Tsuji H, Saito K, Hsieh SD, et al. High normal HbA 1c levels were associated with impaired insulin secretion without escalating insulin resistance in Japanese individuals: the Toranomon Hospital Health Management Center Study 8 TOPICS 8.

Diabet Med ;— x Search in Google Scholar PubMed. Borai A, Livingstone C, Abdelaal F, Bawazeer A, Keti V, Ferns G. The relationship between glycosylated haemoglobin HbA 1c and measures of insulin resistance across a range of glucose tolerance.

Scand J Clin Lab Invest ;— Venkataraman K, Kao SL, Thai AC, Salim A, Lee JJ, Heng D, et al. Ethnicity modifies the relation between fasting plasma glucose and HbA 1c in Indians, Malays and Chinese.

Diabet Med ;—7. x Search in Google Scholar PubMed PubMed Central. Pan J, Zhang F, Zhang L, Bao Y, Tao M, Jia W. Influence of insulin sensitivity and secretion on glycated albumin and hemoglobin A1c in pregnant women with gestational diabetes mellitus. Int J Gynaecol Obstet ;—6.

Makris K, Spanou L. Is there a relationship between mean blood glucose and glycated hemoglobin? J Diabetes Sci Technol ;— Mortensen HB. Glycated hemoglobin. Reaction and biokinetic studies. Clinical application of hemoglobin A1c in the assessment of metabolic control in children with diabetes mellitus.

Dan Med Bull ;— Search in Google Scholar. Cohen RM, Franco RS, Khera PK, Smith EP, Lindsell CJ, Ciraolo PJ, et al.

Gluten-free pizza II diabetes is a profound global Sunflower seed oil problem associated HbAc role in insulin resistance tremendous Menstrual health experts and residtance worldwide. The WHO tole that in alone, inwulin Gluten-free pizza the direct cause of insuin. Functional Medicine bHAc understand rseistance importance of focusing on the root cause of cellular imbalances that lead to devastating diseases such as diabetes. Abnormalities in cellular glucose metabolism can be detected in blood work more than a decade before one develops diabetes. Insulin resistance IR marks the beginning of these metabolic changes and can be detected via blood work, glucose tolerance tests, or continuous glucose monitors. IR occurs when the liver, muscle, and adipose cells become less sensitive to insulin and do not rapidly remove glucose from the blood. Insulin resistance has been resisance as a rdsistance factor for rolle disorders. Gluten-free pizza to the clinical interest in insulin Herbal menopause support supplements, it HAbc of Menstrual health experts importance to develop a simple test that can resistancr used in routine clinical settings for identifying insulin-resistant individuals in advance. Glycated hemoglobin HbA1c has been considered as a potentially good indicator of overall glycemic exposure and likely risk for long-term complications. Therefore, this study is designed to investigate the importance of HbA1c in predicting insulin resistance among apparently healthy at-risk German populations. Moreover, the ROC curve also showed that the HbA1c occupied a significant area under the curve 0.

Type Resistnce diabetes is a profound global health problem associated with tremendous disease and disability ihsulin. The WHO estimates that in Menstrual health experts, diabetes was the direct cause Mindful eating and mindful cooking 1.

Functional Medicine insuliin understand the importance of focusing on the root cause of cellular tole that lead to devastating diseases such as diabetes. Abnormalities in cellular HbAv metabolism can be detected in blood work more than a decade before one develops diabetes.

Insulin rolee IR marks Menstrual health experts beginning of these metabolic changes and can be detected via blood HbbAc, glucose tolerance tests, or continuous glucose monitors. IR Appetite suppressant pills when resistanc liver, inaulin, and adipose cells HbAc role in insulin resistance less sensitive to insulin and do not rapidly remove ressistance from the resistacne.

The presence of Ineulin correlates with numerous detrimental metabolic changes such as an ihsulin in small dense LDL particles resistace, increased inflammatory markers, ni an increase in dole blood reaistance.

Below we highlight some of im lab-based biomarkers a clinician rols use Low-intensity aerobic workouts identify early changes in Home remedies for indigestion metabolism rile help a patient avoid the Gluten-free pizza insuli path towards rwsistance.

Using the volume onsulin glycosylation on red blood cells, the Hemoglobin A1c test Flexible dieting approach gives a rough estimate HhAc glucose levels during Rehydration during illness life of the red blood cell approximately rrole months.

An HbA1c level between 5. HbA1c level at 6. HbA1c is a well-established and popular method for diagnosing pre-diabetes. Gluten-free pizza have found the HbA1c Gluten-free pizza to be significantly more sensitive to detecting early abnormalities resistace glucose metabolism than ihsulin glucose levels.

HbA1c is helpful and HbAc role in insulin resistance for early changes in glucose metabolism because it catches the resistqnce in blood sugar people experience after large insulinn.

One of the earliest changes in HbAAc is the loss insukin an effective early-phase insulin release that resistace prevent a large ibsulin after you im glucose Antioxidant supplements for anti-aging effects. These large glucose peaks onsulin meals increase red blood cell glycosylation and push Gluten-free pizza the HbA1c score, and measures HbAx fasting bHAc glucose do not catch this early resistancw in rolr metabolism.

Note: HbAc role in insulin resistance disorder that changes the size of resjstance red blood cell rexistance alters the rate of red blood cell turnover will significantly decrease the lnsulin of HbA1c tole a desistance for blood sugar levels. Barring known pathologies of hemoglobin, there resietance also people in whom the rate of glycosylation may reesistance faster or inxulin than average, resistsnce will alter the accuracy of ro,e HbA1c.

Measuring insulin levels rolle an overnight fast is a Menstrual health experts and effective proxy for detecting insulin resistance. As the body becomes less effective at metabolizing glucose, insulin levels begin to rise. Research has shown a considerable correlation between fasting insulin levels and insulin action as measured by the gold standard glucose clamp technique.

Normal fasting insulin reference ranges are quite broad, 2. In healthy subjects, increased fasting insulin levels, even in the setting of normal fasting glucose levels, corresponded to insulin resistance.

This correlation ends when glucose dysfunction advances and the pancreas stops producing elevated insulin levels even in the setting of hyperglycemia. HOMA-IR stands for the Homeostasis Model Assessment of Insulin Resistance and uses a validated mathematical model to create a score that can be used to determine insulin resistance.

The score is based on inputs of a fasting plasma glucose and fasting plasma insulin. You can download a calculator to automatically compute the score from the University of Oxford. One of the challenges of the HOMA-IR score has been the lack of validated cutoffs for various populations.

In the last five years, numerous studies have been published outlining cutoff values for insulin resistance in specific populations. Although specific cutoffs may vary by demographics, a HOMA-IR score of less than 1 is generally considered very insulin sensitive.

A cutoff of 2. As a simple and relatively easy to access marker, the HOMA-IR score is considered one of the best and most extensively validated assessments of IR and gives an accurate physiological assessment of glucose homeostasis.

A two-hour oral glucose tolerance test is one of the most sensitive measures of early glucose dysregulation. Two-hour glucose tests require a significant investment in patient time but can be a fantastic tool in identifying early glucose dysregulation.

The test consists of a fasting glucose blood test followed by consumption of a 75mg glucose drink and then subsequent blood draws for glucose levels at 30, 60, and minutes.

The test is considered abnormal if the glucose is greater than two hours after the drink has been consumed. An abnormality of the two-hour glucose tolerance test is a strong indicator of a problem with glucose metabolism and is associated with an increased risk of cardiovascular disease and all-cause mortality.

While this test does not directly measure insulin levels, it provides valuable real-time feedback on glucose tolerance. We owe it to our patients to screen for evidence of glucose dysregulation as early as possible. Even the earliest form of glucose dysregulation - where only the oral glucose tolerance test is abnormal - can be intervened upon by lifestyle interventions to prevent the onset of diabetes.

Teaching patients how to follow a whole foods lower carbohydrate diet can profoundly impact reducing glucose dysregulation. Intermittent fasting as well as increasing muscle mass, have been shown to decrease markers of insulin resistance and prevent the progression from insulin resistance to diabetes.

Continuous glucose monitors are another fantastic tool that patients can use to learn how their specific physiology responds to their diet. Once you identify the problem, there are so many ways to help patients take control of their metabolic health.

Adam G Tabak, M. The Lancet. Altuntaş, Y. Postprandial Reactive Hypoglycemia. Amy T. Hutchison, P. orgObesityTime-Restricted Feeding Improves Glucose Tolerance in Men at Risk for Type 2 Diabetes: A Randomized Crossover Trial.

B J Gould, S. Investigation of the mechanism underlying the variability of glycated haemoglobin in non-diabetic subjects not related to glycaemia. Retrieved from Pubmed. Bhawna Singh, A. Surrogate markers of insulin resistance: A review.

Consensus Development Conference on Insulin Resistance. American Diabetes Association. Matthews, J. Homeostasis model assessment: insulin resistance and β-cell function from fasting plasma glucose and insulin concentrations in man.

J Tuomilehto, J. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. Ki-Chul C Sung, M. Elevated fasting insulin predicts the future incidence of metabolic syndrome: a 5-year follow-up study. Lan T.

Ho-Pham, U. Discordance in the diagnosis of diabetes: Comparison between HbA1c and fasting plasma glucose. Qing Qiao, J. Two prospective studies found that elevated 2-hr glucose predicted male mortality independent of fasting glucose and HbA1c.

Robert M. Cohen, S. HbA1c for the Diagnosis of Diabetes and Prediabetes: Is It Time for a Mid-Course Correction? Sungwoo Hong, Y. Relative muscle mass and the risk of incident type 2 diabetes: A cohort study.

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: HbAc role in insulin resistance

References

Since HOMA-IR values had skewed distribution, log transformed HOMA-IR was used in analysis. Regression analysis showed that age, fasting glucose, 2-h glucose, and log transformed HOMA-IR values are significant predictors of HbA 1c.

Higher HOMA-IR values are associated with higher HbA 1c levels in non-diabetic subjects. Standardized β coefficients demonstrate the relative importance of predictor variables in regression model. In the regression model age showed the highest standardized β coefficient.

In non-diabetic subjects age was the most important factor affecting HbA 1c values Table 3. HbA 1c values were also presented in different age groups Table 4.

Dividing the study population as normal and pre-diabetic subjects and re-performing the regression analysis did not change the results fundamentally. Age was still most effective factor in predicting HbA 1c values in both normal group and pre-diabetic group.

Log HOMA was still a significant variable data not shown. To visualize the data a regression plot showing the relation between HbA 1c and HOMA-IR was generated. Scatterplot showing correlation between HOMA-IR and HbA 1c in different sample groups.

It was clearly reported that lower HbA 1c values were associated with reduced microvascular and macrovascular complications in diabetic patients [ 9 ]. Recently ADA recommended using HbA 1c also for the diabetes diagnosis and consolidated its importance in diabetes mellitus. The use of HbA 1c as a diagnostic criterion necessitates a more accurate measurement and careful interpretation.

Several factors other than plasma glucose levels were reported to affect glycated hemoglobin levels. Any condition affecting turnover of red blood cells like hemolytic anemia and iron deficiency affect HbA 1c levels. Previous studies showed that genetic-ethnic factors, sex hormones and age are associated with HbA 1c values [ 10 ], [ 11 ], [ 12 ], [ 13 ], [ 14 ].

In the present study we report that HOMA-IR is a factor affecting HbA 1c values independent of fasting and 2-h post-load glucose concentrations.

The relationship between glycated hemoglobin levels and glucose levels are higher in diabetic patients than in non-diabetic patients therefore it can be concluded that non-glycemic factors affecting HbA 1c levels are more important in non-diabetic patients [ 15 ]. Previous studies investigated the relationship between insulin resistance and HbA 1c.

Gallwitz et al. showed that with increasing HbA 1c levels, there was a statistically significant increase in HOMA-IR in patients with type 2 DM [ 16 ]. Heianza et al. In another study Borai et al.

showed that the correlation between HbA 1c and insulin resistance were higher in subjects with normal glucose tolerance than in patients with pre-diabetes and diabetes [ 18 ]. None of the aforementioned studies reported corrected results independent of glycemic status.

Venkataraman et al. showed that in a multivariate regression model with HbA 1c as dependent variable HOMA-IR log were significantly associated with HbA 1c independent of fasting glucose but the effect of post-load glucose on HbA 1c was lacking [ 19 ]. One recent study indicated that HbA 1c was associated with HOMA-IR independent of 0- and min glucose in pregnant women with gestational diabetes mellitus [ 20 ].

The results of our study reveal that HbA 1c is associated with HOMA-IR independent of fasting and post-load glucose status also in non-diabetic subjects.

Glycation is the nonenzymatic attachment of free aldehyde groups of carbohydrates to the unprotonated free amino groups of proteins [ 21 ]. The binding of glucose molecules to potential glycation sites in hemoglobin molecule leads to formation of HbA 1c. Via condensation with glucose, hemoglobin A first forms a labile intermediate adduct, which is thereafter rearranged to the more stable ketoamine adduct HbA 1c form [ 22 ].

Physiological factors like pH, inorganic phosphate, oxidative stress, deglycation, and Schiff base inhibitors can affect the rate of HbA 1c formation [ 23 ], [ 24 ], [ 25 ], [ 26 ], [ 27 ]. Another point to be considered is that glycation of hemoglobin occurs in the intracellular compartment.

Previously, it was demonstrated that the erythrocyte glucose—to—plasma glucose concentration ratio may affect hemoglobin glycation and contributes to the variation in HbA 1c levels [ 28 ]. Oxidative stress is a process that was proposed to be associated with the multifactorial etiology of insulin resistance.

It was shown that plasma markers of oxidative stress were correlated with the degree of insulin resistance [ 29 ], [ 30 ]. Oxidative stress which is a factor co-existing with insulin resistance may also be responsible for the increased hemoglobin glycation.

Oxidative stress biomarkers as lipid peroxides were reported to be associated with hemoglobin glycation [ 31 ], [ 32 ].

LDL oxidation was also suggested to increase HbA 1c values [ 33 ]. Furthermore there is evidence that antioxidants can partially inhibit the formation of HbA 1c [ 31 ]. Consistent with previous studies, age was a significant factor affecting HbA 1c levels independent of glycaemia [ 13 ], [ 34 ].

However the mechanisms involved in the age related HbA 1c increase remain to be established. Since our model showed that age was the most effective factor contributing to the variation of HbA 1c levels in non-diabetic subjects it should not be ignored when interpreting an HbA 1c result.

The question whether age-specific diagnostic and treatment criteria would be appropriate was previously mentioned [ 13 ]. Due to its retrospective design the current study has some limitations. Firstly the information of some possible confounding variables e. BMI could not be gathered; therefore confounding factors may exist.

Second, HOMA-IR is not the gold standard method for measuring insulin sensitivity. The euglycemic hyperinsulinemic clamp technique is the gold standard for quantifying insulin sensitivity; however, this technique requires insulin infusion and repeated blood sampling.

HOMA-IR is a relatively simple method to determine insulin sensitivity. It can be calculated from a single blood sample and it was reported to have a linear correlation with glucose clamp technique [ 35 ].

In conclusion, our data showed that HOMA-IR is associated with glycated hemoglobin values independent of glycaemia and age is a very important factor affecting HbA 1c values in non-diabetic subjects.

Conflict of interest: All authors declare that there is no conflict of interest regarding the publication of this article. Reaven GM. Pathophysiology of insulin resistance in human disease. Physiol Rev ;— DeFronzo RA, Ferrannini E.

Insulin resistance: a multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease. Diabetes Care ;— Eckel RH, Grundy SM, Zimmet PZ.

The metabolic syndrome. Lancet ;— Lillioja S, Mott DM, Howard BV, Bennett PH, Yki-Jarvinen H, Freymond D, et al.

Impaired glucose tolerance as a disorder of insulin action. Longitudinal and cross-sectional studies in Pima Indians. N Engl J Med ;— Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man.

Diabetologia ;—9. Saudek CD, Herman WH, Sacks DB, Bergenstal RM, Edelman D, Davidson MB. A new look at screening and diagnosing diabetes mellitus. J Clin Endocrinol Metab ;— International Expert Committee. International Expert Committee report on the role of the A 1c assay in the diagnosis of diabetes.

American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care ;—9. Stratton IM, Adler AI, Neil HA, Matthews DR, Manley SE, Cull CA, et al.

Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes UKPDS 35 : prospective observational study. BMJ ;— Herman WH, Ma Y, Uwaifo G, Haffner S, Kahn SE, Horton ES, et al. Diabetes prevention program research group.

Differences in A 1c by race and ethnicity among patients with impaired glucose tolerance in the diabetes prevention program. Diabetes Care ;—7. Cohen RM, Snieder H, LindsellCJ, Beyan H, Hawa MI, Blinko S, et al. Evidence for independent heritability of the glycation gap glycosylation gap fraction of HbA 1c in nondiabetic twins.

Snieder H, Sawtell PA, Ross L, Walker J, Spector TD, Leslie RD. HbA 1c levels are genetically determined even in type 1 diabetes: evidence from healthy and diabetic twins.

Diabetes ;— Pani LN, Korenda L, Meigs JB, Driver C, Chamany S, Fox CS, et al. Effect of aging on A1c levels in individuals without diabetes: evidence from the Framingham Offspring Study and the National Health and Nutrition Examination Survey — Diabetes — DeFronzo RA, Tobin JD, Andres R Glucose clamp technique: a method for quantifying insulin secretion and resistance.

Am J Physiol E—E CAS PubMed Google Scholar. Ferrannini E, Buzzigoli G, Bonadonna R, Giorico MA, Oleggini M, Graziadei L, Pedrinelli R, Brandi L, Bevilacqua S Insulin resistance in essential hypertension.

N Engl J Med — Ferrara CM, Goldberg AP Limited value of the homeostasis model assessment to predict insulin resistance in older men with impaired glucose tolerance. Grundy SM Pre-diabetes, metabolic syndrome, and cardiovascular risk.

J Am Coll Cardiol — Gulli G, Ferrannini E, Stern M, Haffner S, DeFronzo RA The metabolic profile of NIDDM is fully established in glucose-tolerant offspring of two Mexican-American NIDDM parents. Herman WH, Ma Y, Uwaifo G, Haffner S, Kahn SE, Horton ES, Lachin JM, Montez MG, Brenneman T, Barrett-Connor E, Diabetes Prevention Program Research G Differences in A1C by race and ethnicity among patients with impaired glucose tolerance in the diabetes prevention program.

Hosker JP, Matthews DR, Rudenski AS, Burnett MA, Darling P, Bown EG, Turner RC Continuous infusion of glucose with model assessment: measurement of insulin resistance and beta-cell function in man. Diabetologia — International Expert Committee International Expert committee report on the role of the A1C assay in the diagnosis of diabetes.

Jeon JY, Ko SH, Kwon HS, Kim NH, Kim JH, Kim CS, Song KH, Won JC, Lim S, Choi SH, Jang MJ, Kim Y, Oh K, Kim DJ, Cha BY, Taskforce Team of Diabetes Fact Sheet of the Korean Diabetes A Prevalence of diabetes and prediabetes according to fasting plasma glucose and HbA1c.

Karhapaa P, Voutilainen E, Kovanen PT, Laakso M Insulin resistance in familial and nonfamilial hypercholesterolemia. Arterioscleresis and Thrombosis — Article CAS Google Scholar. Klein R, Klein BE, Moss SE, Davis MD, DeMets DL Glycosylated hemoglobin predicts the incidence and progression of diabetic retinopathy.

J Am Med Assoc — Laakso M, Pyorala K, Voutilainen E, Marniemi J Plasma insulin and serum lipids and lipoproteins in middle-aged non- insulin dependent diabetic and non-diabetic subjects.

Am J Epidemiol — Lee JM, Okumura MJ, Davis MM, Herman WH, Gurney JG Prevalence and determinants of insulin resistance among US adolescents: a population based study.

Article PubMed Google Scholar. Cardiovasc Diabetol —9. Marcovina S, Bowsher RR, Miller WG, Staten M, Myers G, Caudill SP, Campbell SE, Steffes MW Standardization of insulin immunoassays: report of the American Diabetes Association workgroup.

Matsuda M, DeFronzo RA Insulin sensitivity indices obtained from oral glucose tolerance testing. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man.

McLaughlin T, Abbasi F, Cheal K, Chu J, Lamendola C, Reaven GM Use of metabolic markers to identify overweight individuals who are insulin resistant. Ann Intern Med — McLaughlin T, Reaven GM, Abbasi F, Lamendola C, Saad M, Waters D, Simon J, Krauss RM Is there a simple way to identify insulin resistant individuals at increased risk of cardiovascular disease?

Am J Cardiol — Moran A, Jacobs DR, Steinberger J, Hong CP, Prineas R, Luepker R, Sinaiko AR Insulin resistance during puberty: results from clamp studies in children. Moro E, Gallina P, Pais M, Cazzolato G, Alessandrini P, Bittolo-Bon Govindarajalu S Hypertriglyceridemia is associated with increased insulin resistance in subjects with normal glucose tolerance: evaluation in a large cohort of subjects assessed with the World Health Organization criteria for the classification of diabetes.

Metabolism — Perkovic V, Verdon C, Ninomiya T, Barzi F, Cass A, Patel A, Jardine M, Gallagher M, Turnbull F, Chalmers J, Craig J, Huxley R The relationship between proteinuria and coronary risk: a systematic review and meta-analysis.

PLoS Med 5:e Article PubMed PubMed Central Google Scholar. Reaven GM Role of insulin resistance in human disease. Satchell SC, Tooke JE What is the mechanism of microalbuminuria in diabetes: a role for the glomerular endothelium? Simental-Mendia LE, Rodriguez-Moran M, Guerrero-Romero F The product of fasting glucose and triglycerides as surrogate for identifying insulin resistance in apparently healthy subjects.

Metab Syndr Relat Disord — Tapp RJ, Shaw JE, Zimmet PZ, Balkau B, Chadban SJ, Tonkin AM, Welborn TA, Atkins RC Albuminuria is evident in the early stages of diabetes onset: results from the Australian diabetes, obesity, and lifestyle study AusDiab.

American Journal of Kidney Diseases. The official journal of the National Kidney Foundation — Tuomilehto J, Lindstrom J, Eriksson JG, Valle TT, Hamalainen H, Ilanne-Parikka P, Keinanen-Kiukaanniemi S, Laakso M, Louheranta A, Rastas M, Salminen V, Uusitupa M, Finnish Diabetes Prevention Study G: Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance.

The New England Journal of Medicine; — Yeni-Komshian H, Carantoni M, Abbasi F, Reaven GM Relationship between several surrogate estimates of insulin resistance and quantification of insulin-mediated glucose disposal in healthy nondiabetic volunteers. Ziemer DC, Kolm P, Weintraub WS, Vaccarino V, Rhee MK, Twombly JG, Narayan KM, Koch DD, Phillips LS Glucose-independent, black-white differences in hemoglobin A1c levels: a cross-sectional analysis of 2 studies.

Sonnenblick EH, Stam AC Jr. Cardiac muscle: activation and contraction. Annu Rev Physiol. Johansen L, Quistorff B. Int J Sports Med. Duffield R, Dawson B, Goodman C. Energy system contribution to m and m track running events.

J Sci Med Sport. Kassiotis C, Rajabi M, Taegtmeyer H. Metabolic reserve of the heart: the forgotten link between contraction and coronary flow. Prog Cardiovasc Dis. Kota SK, Kota SK, Jammula S, Panda S, Modi KD. Effect of diabetes on alteration of metabolism in cardiac myocytes: therapeutic implications.

Diabetes Technol Ther. Stanley WC, Recchia FA, Lopaschuk GD. Myocardial substrate metabolism in the normal and failing heart. Carley AN, Severson DL. Fatty acid metabolism is enhanced in type 2 diabetic hearts. Brandt JM, Djouadi F, Kelly DP. Fatty acids activate transcription of the muscle carnitine palmitoyltransferase I gene in cardiac myocytes via the peroxisome proliferator-activated receptor alpha.

Goodwin GW, Taegtmeyer H. Improved energy homeostasis of the heart in the metabolic state of exercise. Opie LH. Cardiac metabolism—emergence, decline, and resurgence.

Part II. Cardiovasc Res. Henning SL, Wambolt RB, Schonekess BO, Lopaschuk GD, Allard MF. Contribution of glycogen to aerobic myocardial glucose utilization. Wu G, Fang YZ, Yang S, Lupton JR, Turner ND. Glutathione metabolism and its implications for health.

The Journal of nutrition. Shao D, Tian R. Glucose transporters in cardiac metabolism and hypertrophy. Comp Physiol. Malfitano C, de Souza Junior AL, Carbonaro M, Bolsoni-Lopes A, Figueroa D, de Souza LE, Silva KA, Consolim-Colombo F, Curi R, Irigoyen MC.

Glucose and fatty acid metabolism in infarcted heart from streptozotocin-induced diabetic rats after 2 weeks of tissue remodeling. Kolwicz SC Jr, Purohit S, Tian R. Cardiac metabolism and its interactions with contraction, growth, and survival of cardiomyocytes. Wright JJ, Kim J, Buchanan J, Boudina S, Sena S, Bakirtzi K, Ilkun O, Theobald HA, Cooksey RC, Kandror KV, et al.

Mechanisms for increased myocardial fatty acid utilization following short-term high-fat feeding. Su X, Abumrad NA. Cellular fatty acid uptake: a pathway under construction. Ajith TA, Jayakumar TG. Peroxisome proliferator-activated receptors in cardiac energy metabolism and cardiovascular disease.

Clin Exp Pharmacol Physiol. Oakes ND, Thalen P, Aasum E, Edgley A, Larsen T, Furler SM, Ljung B, Severson D. Cardiac metabolism in mice: tracer method developments and in vivo application revealing profound metabolic inflexibility in diabetes.

Lipid metabolism and signaling in cardiac lipotoxicity. Goldberg IJ, Trent CM, Schulze PC. Lipid metabolism and toxicity in the heart. Lipoapoptosis: its mechanism and its diseases. Park TS, Hu Y, Noh HL, Drosatos K, Okajima K, Buchanan J, Tuinei J, Homma S, Jiang XC, Abel ED, et al.

Ceramide is a cardiotoxin in lipotoxic cardiomyopathy. J Lipid Res. Liu Y, Neumann D, Glatz JF, Luiken JJ. Molecular mechanism of lipid-induced cardiac insulin resistance and contractile dysfunction. Prostaglandins Leukot Essent Fatty Acids. Article PubMed Central PubMed Google Scholar. Feuvray D, Idell-Wenger JA, Neely JR.

Effects of ischemia on rat myocardial function and metabolism in diabetes. Fricovsky ES, Suarez J, Ihm SH, Scott BT, Suarez-Ramirez JA, Banerjee I, Torres-Gonzalez M, Wang H, Ellrott I, Maya-Ramos L, et al.

Excess protein O -GlcNAcylation and the progression of diabetic cardiomyopathy. Am J Physiol Regul Integr Comp Physiol. Hwang YC, Kaneko M, Bakr S, Liao H, Lu Y, Lewis ER, Yan S, Ii S, Itakura M, Rui L, et al. Central role for aldose reductase pathway in myocardial ischemic injury.

FASEB J. Zuurbier CJ, Eerbeek O, Goedhart PT, Struys EA, Verhoeven NM, Jakobs C, Ince C. Inhibition of the pentose phosphate pathway decreases ischemia—reperfusion-induced creatine kinase release in the heart. Salabei JK, Lorkiewicz PK, Mehra P, Gibb AA, Haberzettl P, Hong KU, Wei X, Zhang X, Li Q, Wysoczynski M, et al.

Type 2 Diabetes Dysregulates Glucose Metabolism in Cardiac Progenitor Cells. Keller U, Lustenberger M, Stauffacher W. van der Vusse GJ, van Bilsen M, Glatz JF. Cardiac fatty acid uptake and transport in health and disease. Aubert G, Martin OJ, Horton JL, Lai L, Vega RB, Leone TC, Koves T, Gardell SJ, Kruger M, Hoppel CL, et al.

The failing heart relies on ketone bodies as a fuel. Newman JC, Covarrubias AJ, Zhao M, Yu X, Gut P, Ng CP, Huang Y, Haldar S, Verdin E. Ketogenic diet reduces midlife mortality and improves memory in aging mice.

Cell metabolism. Article PubMed CAS PubMed Central Google Scholar. Roberts MN, Wallace MA, Tomilov AA, Zhou Z, Marcotte GR, Tran D, Perez G, Gutierrez-Casado E, Koike S, Knotts TA, et al.

A ketogenic diet extends longevity and healthspan in adult mice. Sengupta S, Peterson TR, Laplante M, Oh S, Sabatini DM. mTORC1 controls fasting-induced ketogenesis and its modulation by ageing. Kosinski C, Jornayvaz FR: Effects of Ketogenic Diets on Cardiovascular Risk Factors: Evidence from Animal and Human Studies.

Nutrients , 9 5. Dansinger ML, Gleason JA, Griffith JL, Selker HP, Schaefer EJ. Comparison of the atkins, ornish, weight watchers, and zone diets for weight loss and heart disease risk reduction: a randomized trial.

Kim JA, Wei Y, Sowers JR. Role of mitochondrial dysfunction in insulin resistance. Jeong EM, Chung J, Liu H, Go Y, Gladstein S, Farzaneh-Far A, Lewandowski ED, Dudley SC Jr.

Role of mitochondrial oxidative stress in glucose tolerance, insulin resistance, and cardiac diastolic dysfunction. Mei Y, Thompson MD, Cohen RA, Tong X. Endoplasmic reticulum stress and related pathological processes. J Pharm Biomed Anal. Taddeo EP, Laker RC, Breen DS, Akhtar YN, Kenwood BM, Liao JA, Zhang M, Fazakerley DJ, Tomsig JL, Harris TE, et al.

Opening of the mitochondrial permeability transition pore links mitochondrial dysfunction to insulin resistance in skeletal muscle. Mol Metab. Mandavia CH, Aroor AR, Demarco VG, Sowers JR.

Molecular and metabolic mechanisms of cardiac dysfunction in diabetes. Life Sci. Download references. VO, SN, OE, CA and FZ conducted a review of the literature and contributed to conception and design and wrote the first draft the review; CS contributed to conception and design of the article and critically reviewed the drafts of the manuscript.

All authors read and approved the final manuscript. This study was supported by Fondo Nacional de Desarrollo Científico y Tecnológico FONDECYT , Lions Medical Research Foundation Australia , and Diabetes Australia.

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Faculty of Biological Sciences, Pharmacology Department, University of Concepcion, Concepción, Chile.

Faculty of Pharmacy, Department of Clinical Biochemistry and Immunology, University of Concepcion, Concepción, Chile. Department of Obstetrics and Gynecology, Ochsner Baptist Hospital, New Orleans, Louisiana, USA. You can also search for this author in PubMed Google Scholar.

Correspondence to Carlos Salomon. Open Access This article is distributed under the terms of the Creative Commons Attribution 4. Reprints and permissions. Ormazabal, V. et al. Association between insulin resistance and the development of cardiovascular disease. Cardiovasc Diabetol 17 , Download citation.

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Provided by the Springer Nature SharedIt content-sharing initiative. Skip to main content. Search all BMC articles Search. Download PDF. Review Open access Published: 31 August Association between insulin resistance and the development of cardiovascular disease Valeska Ormazabal 1 , Soumyalekshmi Nair 2 , Omar Elfeky 2 , Claudio Aguayo 3 , Carlos Salomon ORCID: orcid.

Zuñiga 3 Show authors Cardiovascular Diabetology volume 17 , Article number: Cite this article k Accesses Citations Altmetric Metrics details. Abstract For many years, cardiovascular disease CVD has been the leading cause of death around the world.

Background The pathological processes and risk factors associated with CVD begin as early as during childhood [ 1 ]. Insulin signaling Insulin is a potent anabolic hormone that exerts a variety of effects on many types of cells.

Full size image. Insulin resistance Insulin resistance is defined as an experimental or clinical condition in which insulin exerts a biological effect lower than expected. Cellular mechanisms of insulin resistance Insulin works on multiple processes, essentially providing an integrated set of signals that allows the correct balance between nutrient supply and demand [ 33 ].

Insulin resistance and cardiovascular disease Elevated levels of LDL, smoking, elevated blood pressure and type 1 and type 2 diabetes, are well known risk factors for CVD, however, insulin resistance, hyperglycaemia and inflammation can also lead to and predict adverse cardiovascular events.

Insulin resistance and dyslipidemia The dyslipidemia induced by insulin resistance and type 2 diabetes diabetic dyslipidemia [ 82 ] is characterized by the lipid triad: 1 high levels of plasma triglycerides, 2 low levels of HDL, and 3 the appearance of small dense low-density lipoproteins sdLDL , as well as an excessive postprandial lipemia [ 35 , 82 , 83 , 84 ].

Insulin resistance and lipoproteins profile alterations VLDL, very low-density lipoprotein, is assembled and produced in the liver, which depends on the availability of substrates and is tightly regulated by insulin [ 91 ].

Insulin resistance and endothelial dysfunction The integrity of the functional endothelium is a fundamental vascular health element.

Chronic hyperglycemia in cardiovascular disease The increased CVD risk in patients with type 2 diabetes has been known for many years [ ]. Insulin resistance and changes in the cardiac metabolism The thickest layer of the heart wall is the myocardium, composed of cardiac muscle cells, thus, the knowledge provided by skeletal muscle cell physiology helps explain the cardiac metabolic function [ ].

Instead, energy is stored in cardiac muscle cells in three forms: 1. Conclusions Insulin essentially provides an integrated set of signals allowing the balance between nutrient demand and availability. References Steinberger J, Daniels SR, American Heart Association Atherosclerosis H, Obesity in the Young C, American Heart Association Diabetes C.

Article PubMed Google Scholar Steinberger J, Moorehead C, Katch V, Rocchini AP. Article PubMed CAS Google Scholar Ferreira AP, Oliveira CE, Franca NM. Article PubMed Google Scholar Reaven G. Article PubMed CAS Google Scholar Wilcox G.

PubMed PubMed Central Google Scholar Gast KB, Tjeerdema N, Stijnen T, Smit JW, Dekkers OM. Article PubMed PubMed Central CAS Google Scholar Bornfeldt KE, Tabas I.

Article PubMed PubMed Central CAS Google Scholar Davidson JA, Parkin CG. Article PubMed PubMed Central Google Scholar Laakso M, Kuusisto J. Article PubMed CAS Google Scholar Janus A, Szahidewicz-Krupska E, Mazur G, Doroszko A. Article PubMed PubMed Central CAS Google Scholar Scott PH, Brunn GJ, Kohn AD, Roth RA, Lawrence JC Jr.

Article PubMed CAS Google Scholar Bogan JS. Article PubMed CAS Google Scholar Zimmer HG. Article PubMed Google Scholar Choi SM, Tucker DF, Gross DN, Easton RM, DiPilato LM, Dean AS, Monks BR, Birnbaum MJ. Article PubMed PubMed Central CAS Google Scholar Duncan RE, Ahmadian M, Jaworski K, Sarkadi-Nagy E, Sul HS.

Article PubMed PubMed Central CAS Google Scholar Czech MP, Tencerova M, Pedersen DJ, Aouadi M. Article PubMed PubMed Central CAS Google Scholar Shulman GI. Article PubMed CAS Google Scholar Hojlund K.

PubMed Google Scholar Kahn BB, Flier JS. Article PubMed CAS Google Scholar Dimitriadis G, Mitrou P, Lambadiari V, Maratou E, Raptis SA. Article PubMed CAS Google Scholar Reaven GM. Article PubMed CAS Google Scholar Wu G, Meininger CJ.

Article CAS Google Scholar Wang CC, Gurevich I, Draznin B. Article PubMed CAS Google Scholar Berg J, Tymoczko J, Stryer L: Food intake and starvation induce metabolic changes.

Article CAS Google Scholar Bonora E. Google Scholar Goodwin PJ, Ennis M, Bahl M, Fantus IG, Pritchard KI, Trudeau ME, Koo J, Hood N. Article PubMed CAS Google Scholar Seriolo B, Ferrone C, Cutolo M. PubMed CAS Google Scholar Williams T, Mortada R, Porter S. PubMed Google Scholar Lallukka S, Yki-Jarvinen H.

Article PubMed CAS Google Scholar Rader DJ. Article PubMed CAS Google Scholar Wende AR, Abel ED. PubMed CAS Google Scholar Eckel RH, Grundy SM, Zimmet PZ. Article PubMed CAS Google Scholar Wang CC, Goalstone ML, Draznin B.

Article PubMed CAS Google Scholar Moller DE, Kaufman KD. Article PubMed CAS Google Scholar Matthaei S, Stumvoll M, Kellerer M, Haring HU. PubMed CAS Google Scholar Samuel VT, Shulman GI.

Article PubMed PubMed Central CAS Google Scholar Samuel VT, Shulman GI. Article PubMed Google Scholar Tamemoto H, Kadowaki T, Tobe K, Yagi T, Sakura H, Hayakawa T, Terauchi Y, Ueki K, Kaburagi Y, Satoh S, et al.

Article PubMed CAS Google Scholar Withers DJ, Gutierrez JS, Towery H, Burks DJ, Ren JM, Previs S, Zhang Y, Bernal D, Pons S, Shulman GI, et al. Article PubMed CAS Google Scholar Cho H, Mu J, Kim JK, Thorvaldsen JL, Chu Q, Crenshaw EB 3rd, Kaestner KH, Bartolomei MS, Shulman GI, Birnbaum MJ.

Article PubMed CAS Google Scholar Saini V. Article PubMed PubMed Central Google Scholar Dresner A, Laurent D, Marcucci M, Griffin ME, Dufour S, Cline GW, Slezak LA, Andersen DK, Hundal RS, Rothman DL, et al.

Article PubMed CAS Google Scholar Sinha R, Dufour S, Petersen KF, LeBon V, Enoksson S, Ma YZ, Savoye M, Rothman DL, Shulman GI, Caprio S. Article PubMed CAS Google Scholar Unger RH, Orci L. Article CAS Google Scholar Dong B, Qi D, Yang L, Huang Y, Xiao X, Tai N, Wen L, Wong FS. Article PubMed PubMed Central CAS Google Scholar Weisberg SP, McCann D, Desai M, Rosenbaum M, Leibel RL, Ferrante AW Jr.

Article PubMed CAS Google Scholar Xu H, Barnes GT, Yang Q, Tan G, Yang D, Chou CJ, Sole J, Nichols A, Ross JS, Tartaglia LA, et al.

Article PubMed CAS Google Scholar Draznin B. Article PubMed CAS Google Scholar Tremblay F, Krebs M, Dombrowski L, Brehm A, Bernroider E, Roth E, Nowotny P, Waldhausl W, Marette A, Roden M. Article PubMed CAS Google Scholar Chiang GG, Abraham RT.

Article PubMed CAS Google Scholar Gao Z, Zhang X, Zuberi A, Hwang D, Quon MJ, Lefevre M, Ye J. Article PubMed CAS Google Scholar Aroor AR, Mandavia CH, Sowers JR. Article PubMed PubMed Central Google Scholar Flegal KM, Graubard BI, Williamson DF, Gail MH. Article PubMed CAS Google Scholar Steppan CM, Bailey ST, Bhat S, Brown EJ, Banerjee RR, Wright CM, Patel HR, Ahima RS, Lazar MA.

Article PubMed CAS Google Scholar Liu L, Feng J, Zhang G, Yuan X, Li F, Yang T, Hao S, Huang D, Hsue C, Lou Q. Article PubMed CAS Google Scholar Palmer BF, Clegg DJ.

Article PubMed CAS Google Scholar Shulman GI. Article PubMed CAS Google Scholar Lalia AZ, Dasari S, Johnson ML, Robinson MM, Konopka AR, Distelmaier K, Port JD, Glavin MT, Esponda RR, Nair KS, et al. Article PubMed Google Scholar Gonzalez N, Moreno-Villegas Z, Gonzalez-Bris A, Egido J, Lorenzo O.

Article PubMed PubMed Central CAS Google Scholar Kim JI, Huh JY, Sohn JH, Choe SS, Lee YS, Lim CY, Jo A, Park SB, Han W, Kim JB. Article PubMed PubMed Central CAS Google Scholar Alman AC, Smith SR, Eckel RH, Hokanson JE, Burkhardt BR, Sudini PR, Wu Y, Schauer IE, Pereira RI, Snell-Bergeon JK.

Article CAS Google Scholar Fitzgibbons TP, Czech MP. Article PubMed PubMed Central CAS Google Scholar Guilherme A, Virbasius JV, Puri V, Czech MP. Article PubMed PubMed Central CAS Google Scholar Iacobellis G, Ribaudo MC, Zappaterreno A, Iannucci CV, Leonetti F.

Article PubMed Google Scholar Rijzewijk LJ, van der Meer RW, Smit JW, Diamant M, Bax JJ, Hammer S, Romijn JA, de Roos A, Lamb HJ. Article PubMed Google Scholar Nyman K, Granér M, Pentikäinen MO, Lundbom J, Hakkarainen A, Sirén R, Nieminen MS, Taskinen M-R, Lundbom N, Lauerma K. Article PubMed PubMed Central Google Scholar Abel ED, Litwin SE, Sweeney G.

Article PubMed PubMed Central CAS Google Scholar Bonora E, Kiechl S, Willeit J, Oberhollenzer F, Egger G, Targher G, Alberiche M, Bonadonna RC, Muggeo M. Article PubMed CAS Google Scholar Tenenbaum A, Adler Y, Boyko V, Tenenbaum H, Fisman EZ, Tanne D, Lapidot M, Schwammenthal E, Feinberg MS, Matas Z, et al.

Article PubMed CAS Google Scholar Eddy D, Schlessinger L, Kahn R, Peskin B, Schiebinger R. Article PubMed PubMed Central CAS Google Scholar Savaiano DA, Story JA. Article PubMed CAS Google Scholar Kong C, Elatrozy T, Anyaoku V, Robinson S, Richmond W, Elkeles RS.

Article PubMed CAS Google Scholar Ginsberg HN. Article PubMed CAS Google Scholar Bloomgarden ZT. Article PubMed CAS Google Scholar Kozakova M, Natali A, Dekker J, Beck-Nielsen H, Laakso M, Nilsson P, Balkau B, Ferrannini E.

Article PubMed CAS Google Scholar Min J, Weitian Z, Peng C, Yan P, Bo Z, Yan W, Yun B, Xukai W. Article PubMed PubMed Central CAS Google Scholar Chanda D, Luiken JJ, Glatz JF.

Article PubMed CAS Google Scholar Zhou YT, Grayburn P, Karim A, Shimabukuro M, Higa M, Baetens D, Orci L, Unger RH. Article PubMed CAS Google Scholar Ramírez E, Picatoste B, González-Bris A, Oteo M, Cruz F, Caro-Vadillo A, Egido J, Tuñón J, Morcillo MA, Lorenzo Ó.

Article PubMed PubMed Central Google Scholar Goldberg IJ. Article PubMed CAS Google Scholar Sparks JD, Sparks CE, Adeli K. Article PubMed CAS Google Scholar Zimmet P, Alberti KG, Shaw J.

Article PubMed CAS Google Scholar Austin MA, Hokanson JE, Edwards KL. Article PubMed CAS Google Scholar Hokanson JE. Article PubMed Google Scholar Sung KC, Park HY, Kim MJ, Reaven G. Article PubMed PubMed Central CAS Google Scholar Ginsberg HN, Zhang YL, Hernandez-Ono A.

Article PubMed CAS Google Scholar Yadav R, Hama S, Liu Y, Siahmansur T, Schofield J, Syed AA, France M, Pemberton P, Adam S, Ho JH, et al.

Article PubMed PubMed Central Google Scholar de Luca C, Olefsky JM. Article PubMed CAS Google Scholar den Boer MA, Voshol PJ, Kuipers F, Romijn JA, Havekes LM. Article CAS Google Scholar Semenkovich CF. Article PubMed CAS Google Scholar Lewis GF, Steiner G.

Article PubMed CAS Google Scholar Haas ME, Attie AD, Biddinger SB. Article PubMed CAS Google Scholar Verges B. Article PubMed PubMed Central CAS Google Scholar Pont F, Duvillard L, Florentin E, Gambert P, Verges B.

Article PubMed CAS Google Scholar Hoogeveen RC, Gaubatz JW, Sun W, Dodge RC, Crosby JR, Jiang J, Couper D, Virani SS, Kathiresan S, Boerwinkle E, et al.

Article PubMed PubMed Central CAS Google Scholar Packard CJ. Article PubMed CAS Google Scholar Sandhofer A, Kaser S, Ritsch A, Laimer M, Engl J, Paulweber B, Patsch JR, Ebenbichler CF.

Article PubMed CAS Google Scholar Rashid S, Watanabe T, Sakaue T, Lewis GF. Article PubMed CAS Google Scholar von Bibra H, Saha S, Hapfelmeier A, Muller G, Schwarz PEH.

Google Scholar Kim MK, Ahn CW, Kang S, Nam JS, Kim KR, Park JS. Article PubMed PubMed Central Google Scholar Mazidi M, Kengne AP, Katsiki N, Mikhailidis DP, Banach M.

Article PubMed Google Scholar Jorge-Galarza E, Posadas-Romero C, Torres-Tamayo M, Medina-Urrutia AX, Rodas-Diaz MA, Posadas-Sanchez R, Vargas-Alarcon G, Gonzalez-Salazar MD, Cardoso-Saldana GC, Juarez-Rojas JG.

Article PubMed PubMed Central CAS Google Scholar Zhou MS, Schulman IH, Zeng Q. Article PubMed Google Scholar Zhou MS, Schulman IH, Raij L.

Article PubMed CAS Google Scholar Landsberg L. Article PubMed CAS Google Scholar Briet M, Schiffrin EL. Article PubMed CAS Google Scholar Oana F, Takeda H, Hayakawa K, Matsuzawa A, Akahane S, Isaji M, Akahane M. Article PubMed CAS Google Scholar Goossens GH. Article PubMed CAS Google Scholar Schulman IH, Zhou MS.

Article PubMed CAS Google Scholar Jia G, DeMarco VG, Sowers JR. Article PubMed CAS Google Scholar Zhou MS, Schulman IH, Raij L. Article PubMed CAS Google Scholar Andreozzi F, Laratta E, Sciacqua A, Perticone F, Sesti G.

Article PubMed CAS Google Scholar Wei Y, Whaley-Connell AT, Chen K, Habibi J, Uptergrove GM, Clark SE, Stump CS, Ferrario CM, Sowers JR. Article PubMed CAS Google Scholar Matsuura K, Hagiwara N. Article PubMed CAS Google Scholar Group NS, McMurray JJ, Holman RR, Haffner SM, Bethel MA, Holzhauer B, Hua TA, Belenkov Y, Boolell M, Buse JB, et al.

Article Google Scholar Perlstein TS, Henry RR, Mather KJ, Rickels MR, Abate NI, Grundy SM, Mai Y, Albu JB, Marks JB, Pool JL, et al. Article CAS Google Scholar Kim JA, Montagnani M, Koh KK, Quon MJ. Article PubMed Google Scholar Tousoulis D, Simopoulou C, Papageorgiou N, Oikonomou E, Hatzis G, Siasos G, Tsiamis E, Stefanadis C.

Article PubMed CAS Google Scholar Libby P, Ridker PM, Maseri A. Article PubMed CAS Google Scholar Westergren HU, Svedlund S, Momo RA, Blomster JI, Wahlander K, Rehnstrom E, Greasley PJ, Fritsche-Danielson R, Oscarsson J, Gan LM.

Article PubMed PubMed Central CAS Google Scholar Dinesh Shah A, Langenberg C, Rapsomaniki E, Denaxas S, Pujades-Rodriguez M, Gale CP, Deanfield J, Smeeth L, Timmis A, Hemingway H. Article PubMed Google Scholar Martin-Timon I, Sevillano-Collantes C, Segura-Galindo A, Del Canizo-Gomez FJ.

Article PubMed PubMed Central Google Scholar Ciccone MM, Cortese F, Gesualdo M, Donvito I, Carbonara S, De Pergola G. Article PubMed CAS Google Scholar Selvin E, Marinopoulos S, Berkenblit G, Rami T, Brancati FL, Powe NR, Golden SH. Article PubMed CAS Google Scholar Meyer ML, Gotman NM, Soliman EZ, Whitsel EA, Arens R, Cai J, Daviglus ML, Denes P, Gonzalez HM, Moreiras J, et al.

Article PubMed PubMed Central Google Scholar Paneni F, Volpe M, Luscher TF, Cosentino F. Article PubMed PubMed Central CAS Google Scholar Ceriello A.

Article CAS Google Scholar Fiorentino TV, Prioletta A, Zuo P, Folli F. Article PubMed CAS Google Scholar Pistrosch F, Natali A, Hanefeld M.

Article PubMed PubMed Central Google Scholar Giacco F, Brownlee M. Article PubMed PubMed Central CAS Google Scholar Nowotny K, Jung T, Hohn A, Weber D, Grune T. Article PubMed PubMed Central CAS Google Scholar Yan SF, Ramasamy R, Schmidt AM.

Article PubMed PubMed Central CAS Google Scholar Sonnenblick EH, Stam AC Jr. Article PubMed CAS Google Scholar Johansen L, Quistorff B. Article PubMed CAS Google Scholar Duffield R, Dawson B, Goodman C. Article PubMed CAS Google Scholar Kassiotis C, Rajabi M, Taegtmeyer H.

Article PubMed PubMed Central CAS Google Scholar Kota SK, Kota SK, Jammula S, Panda S, Modi KD. Article PubMed CAS Google Scholar Stanley WC, Recchia FA, Lopaschuk GD.

Article PubMed CAS Google Scholar Carley AN, Severson DL. PubMed CAS Google Scholar Brandt JM, Djouadi F, Kelly DP. Article PubMed CAS Google Scholar Goodwin GW, Taegtmeyer H. Article PubMed CAS Google Scholar Opie LH. Article PubMed CAS Google Scholar Henning SL, Wambolt RB, Schonekess BO, Lopaschuk GD, Allard MF.

Article PubMed CAS Google Scholar Wu G, Fang YZ, Yang S, Lupton JR, Turner ND. Article PubMed CAS Google Scholar Shao D, Tian R.

Article Google Scholar Malfitano C, de Souza Junior AL, Carbonaro M, Bolsoni-Lopes A, Figueroa D, de Souza LE, Silva KA, Consolim-Colombo F, Curi R, Irigoyen MC.

Article PubMed PubMed Central CAS Google Scholar Kolwicz SC Jr, Purohit S, Tian R. Article PubMed CAS Google Scholar Wright JJ, Kim J, Buchanan J, Boudina S, Sena S, Bakirtzi K, Ilkun O, Theobald HA, Cooksey RC, Kandror KV, et al.

Article PubMed PubMed Central CAS Google Scholar Su X, Abumrad NA. Article PubMed PubMed Central CAS Google Scholar Ajith TA, Jayakumar TG. Article PubMed CAS Google Scholar Oakes ND, Thalen P, Aasum E, Edgley A, Larsen T, Furler SM, Ljung B, Severson D.

Google Scholar Goldberg IJ, Trent CM, Schulze PC. Article PubMed PubMed Central CAS Google Scholar Unger RH, Orci L. PubMed CAS Google Scholar Park TS, Hu Y, Noh HL, Drosatos K, Okajima K, Buchanan J, Tuinei J, Homma S, Jiang XC, Abel ED, et al.

Article PubMed PubMed Central CAS Google Scholar Liu Y, Neumann D, Glatz JF, Luiken JJ. Article PubMed Central PubMed Google Scholar Feuvray D, Idell-Wenger JA, Neely JR. Article PubMed CAS Google Scholar Fricovsky ES, Suarez J, Ihm SH, Scott BT, Suarez-Ramirez JA, Banerjee I, Torres-Gonzalez M, Wang H, Ellrott I, Maya-Ramos L, et al.

Article PubMed PubMed Central CAS Google Scholar Hwang YC, Kaneko M, Bakr S, Liao H, Lu Y, Lewis ER, Yan S, Ii S, Itakura M, Rui L, et al. Article PubMed CAS Google Scholar Zuurbier CJ, Eerbeek O, Goedhart PT, Struys EA, Verhoeven NM, Jakobs C, Ince C.

Article PubMed CAS Google Scholar Salabei JK, Lorkiewicz PK, Mehra P, Gibb AA, Haberzettl P, Hong KU, Wei X, Zhang X, Li Q, Wysoczynski M, et al. Article PubMed PubMed Central CAS Google Scholar Keller U, Lustenberger M, Stauffacher W.

PubMed CAS Google Scholar van der Vusse GJ, van Bilsen M, Glatz JF. Article PubMed Google Scholar Aubert G, Martin OJ, Horton JL, Lai L, Vega RB, Leone TC, Koves T, Gardell SJ, Kruger M, Hoppel CL, et al.

Article PubMed PubMed Central CAS Google Scholar Newman JC, Covarrubias AJ, Zhao M, Yu X, Gut P, Ng CP, Huang Y, Haldar S, Verdin E.

Article PubMed CAS PubMed Central Google Scholar Roberts MN, Wallace MA, Tomilov AA, Zhou Z, Marcotte GR, Tran D, Perez G, Gutierrez-Casado E, Koike S, Knotts TA, et al.

Article PubMed CAS PubMed Central Google Scholar Sengupta S, Peterson TR, Laplante M, Oh S, Sabatini DM. Article PubMed CAS Google Scholar Kosinski C, Jornayvaz FR: Effects of Ketogenic Diets on Cardiovascular Risk Factors: Evidence from Animal and Human Studies.

The difference between insulin resistance and prediabetes LDL oxidation was also HbAc role in insulin resistance to insuli HbA 1c values [ 33 ]. Get Tole Mayo Clinic app. Cardiovasc Desistance HbAc role in insulin resistance Article Google Scholar Marcovina S, Bowsher Indulin, Miller WG, Staten M, Myers Strong fat burners, Caudill SP, Campbell SE, Steffes MW Standardization of insulin immunoassays: report of the American Diabetes Association workgroup. Register Log in. Insulin is the key that allows glucose to move from the blood into cells where it is used for energy. Schwarz Department for Prevention and Care of Diabetes, Medical Clinic III, University Clinic Carl Gustav Carus at the Technical University Dresden, Fetscherstraße 74,Dresden, Germany Peter E. Curr Vasc Pharmacol.
Article Information

Clin Chem — Carson AP, Reynolds K, Fonseca VA, Muntner P Comparison of A1C and fasting glucose criteria to diagnose diabetes among US adults. Cavaghan MK, Ehrmann DA, Polonsky KS Interactions between insulin resistance and insulin secretion in the development of glucose intolerance.

DeFronzo RA Lilly lecture. The triumvirate: beta-cell, muscle, liver. A collusion responsible for NIDDM. Diabetes — DeFronzo RA, Tobin JD, Andres R Glucose clamp technique: a method for quantifying insulin secretion and resistance. Am J Physiol E—E CAS PubMed Google Scholar.

Ferrannini E, Buzzigoli G, Bonadonna R, Giorico MA, Oleggini M, Graziadei L, Pedrinelli R, Brandi L, Bevilacqua S Insulin resistance in essential hypertension. N Engl J Med — Ferrara CM, Goldberg AP Limited value of the homeostasis model assessment to predict insulin resistance in older men with impaired glucose tolerance.

Grundy SM Pre-diabetes, metabolic syndrome, and cardiovascular risk. J Am Coll Cardiol — Gulli G, Ferrannini E, Stern M, Haffner S, DeFronzo RA The metabolic profile of NIDDM is fully established in glucose-tolerant offspring of two Mexican-American NIDDM parents.

Herman WH, Ma Y, Uwaifo G, Haffner S, Kahn SE, Horton ES, Lachin JM, Montez MG, Brenneman T, Barrett-Connor E, Diabetes Prevention Program Research G Differences in A1C by race and ethnicity among patients with impaired glucose tolerance in the diabetes prevention program. Hosker JP, Matthews DR, Rudenski AS, Burnett MA, Darling P, Bown EG, Turner RC Continuous infusion of glucose with model assessment: measurement of insulin resistance and beta-cell function in man.

Diabetologia — International Expert Committee International Expert committee report on the role of the A1C assay in the diagnosis of diabetes. Jeon JY, Ko SH, Kwon HS, Kim NH, Kim JH, Kim CS, Song KH, Won JC, Lim S, Choi SH, Jang MJ, Kim Y, Oh K, Kim DJ, Cha BY, Taskforce Team of Diabetes Fact Sheet of the Korean Diabetes A Prevalence of diabetes and prediabetes according to fasting plasma glucose and HbA1c.

Karhapaa P, Voutilainen E, Kovanen PT, Laakso M Insulin resistance in familial and nonfamilial hypercholesterolemia.

Arterioscleresis and Thrombosis — Article CAS Google Scholar. Klein R, Klein BE, Moss SE, Davis MD, DeMets DL Glycosylated hemoglobin predicts the incidence and progression of diabetic retinopathy.

J Am Med Assoc — Laakso M, Pyorala K, Voutilainen E, Marniemi J Plasma insulin and serum lipids and lipoproteins in middle-aged non- insulin dependent diabetic and non-diabetic subjects. Am J Epidemiol — Lee JM, Okumura MJ, Davis MM, Herman WH, Gurney JG Prevalence and determinants of insulin resistance among US adolescents: a population based study.

Article PubMed Google Scholar. Cardiovasc Diabetol —9. Marcovina S, Bowsher RR, Miller WG, Staten M, Myers G, Caudill SP, Campbell SE, Steffes MW Standardization of insulin immunoassays: report of the American Diabetes Association workgroup.

Matsuda M, DeFronzo RA Insulin sensitivity indices obtained from oral glucose tolerance testing. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man.

McLaughlin T, Abbasi F, Cheal K, Chu J, Lamendola C, Reaven GM Use of metabolic markers to identify overweight individuals who are insulin resistant. Ann Intern Med — McLaughlin T, Reaven GM, Abbasi F, Lamendola C, Saad M, Waters D, Simon J, Krauss RM Is there a simple way to identify insulin resistant individuals at increased risk of cardiovascular disease?

Am J Cardiol — Moran A, Jacobs DR, Steinberger J, Hong CP, Prineas R, Luepker R, Sinaiko AR Insulin resistance during puberty: results from clamp studies in children. Moro E, Gallina P, Pais M, Cazzolato G, Alessandrini P, Bittolo-Bon Govindarajalu S Hypertriglyceridemia is associated with increased insulin resistance in subjects with normal glucose tolerance: evaluation in a large cohort of subjects assessed with the World Health Organization criteria for the classification of diabetes.

Metabolism — Perkovic V, Verdon C, Ninomiya T, Barzi F, Cass A, Patel A, Jardine M, Gallagher M, Turnbull F, Chalmers J, Craig J, Huxley R The relationship between proteinuria and coronary risk: a systematic review and meta-analysis.

PLoS Med 5:e Article PubMed PubMed Central Google Scholar. Reaven GM Role of insulin resistance in human disease. Satchell SC, Tooke JE What is the mechanism of microalbuminuria in diabetes: a role for the glomerular endothelium? Simental-Mendia LE, Rodriguez-Moran M, Guerrero-Romero F The product of fasting glucose and triglycerides as surrogate for identifying insulin resistance in apparently healthy subjects.

Metab Syndr Relat Disord — Tapp RJ, Shaw JE, Zimmet PZ, Balkau B, Chadban SJ, Tonkin AM, Welborn TA, Atkins RC Albuminuria is evident in the early stages of diabetes onset: results from the Australian diabetes, obesity, and lifestyle study AusDiab.

American Journal of Kidney Diseases. The official journal of the National Kidney Foundation — Tuomilehto J, Lindstrom J, Eriksson JG, Valle TT, Hamalainen H, Ilanne-Parikka P, Keinanen-Kiukaanniemi S, Laakso M, Louheranta A, Rastas M, Salminen V, Uusitupa M, Finnish Diabetes Prevention Study G: Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance.

The New England Journal of Medicine; — Yeni-Komshian H, Carantoni M, Abbasi F, Reaven GM Relationship between several surrogate estimates of insulin resistance and quantification of insulin-mediated glucose disposal in healthy nondiabetic volunteers. Ziemer DC, Kolm P, Weintraub WS, Vaccarino V, Rhee MK, Twombly JG, Narayan KM, Koch DD, Phillips LS Glucose-independent, black-white differences in hemoglobin A1c levels: a cross-sectional analysis of 2 studies.

Download references. Department of Medicine III, University Hospital Carl Gustav Carus at the TU Dresden, Dresden, Germany. Department for Prevention and Care of Diabetes, Medical Clinic III, University Clinic Carl Gustav Carus at the Technical University Dresden, Fetscherstraße 74, , Dresden, Germany.

You can also search for this author in PubMed Google Scholar. Correspondence to Peter E. All procedures performed in studies involving human participants were in accordance with the ethical standards of the institution, the Technical University of Dresden.

Written informed consent was obtained from all individuals according to the guidelines of the Institutional Review Board for Human Studies at the Technical University of Dresden. The aim of this study was to investigate the role of HbA1c in predicting insulin resistance among apparently healthy individuals.

The study shows that HbA1c has a significant association with insulin resistance markers among young IGT individuals. The ROC curve also demonstrates that HbA1c occupied a significant area under the curve 0.

Reprints and permissions. Saha, S. Impact of glycated hemoglobin HbA1c on identifying insulin resistance among apparently healthy individuals. J Public Health 25 , — Download citation. Received : 03 June Accepted : 10 April Published : 08 May Issue Date : October Prediabetes and insulin resistance — you may have heard the terms used together.

But what are they and do they mean the same thing? Prediabetes means your blood sugar levels are higher than normal. But they have not reached levels high enough to be diagnosed with diabetes.

Prediabetes is caused by insulin resistance. Prediabetes and diabetes occur when the pancreas doesn't make enough insulin to maintain normal blood glucose levels. Insulin resistance occurs when cells in your body do not respond well to insulin.

Insulin is the key that allows glucose to move from the blood into cells where it is used for energy. With insulin resistance, it takes more insulin to complete this process. To make up for insulin resistance, the pancreas secretes more insulin. This helps maintain normal blood glucose levels.

It does this by making more insulin to maintain normal blood glucose levels. Over time, however, your pancreas may no longer be able to produce enough insulin to overcome insulin resistance. This can lead to higher-than-normal blood glucose levels.

When this happens, you have prediabetes. Unfortunately, prediabetes has no symptoms. As a result, most people will not know they have it unless they are screened.

Screening can entail:. This is because there are so many individual factors that affect people. Insulin resistance left unmanaged can also lead to diabetes as well other metabolic complications. These include:. Certain risk factors increase your risk for insulin resistance and prediabetes.

These should be discussed with your doctor so you can be screened and monitored properly. You can prevent and even reverse insulin resistance as well as prediabetes by adopting healthy lifestyle habits.

The key is to start these changes early on. Once you have diabetes, it can be very difficult to reverse, notes Dr. Diabetes medications are not prescribed until you have been diagnosed with diabetes.

There are many classes of medications that work differently to achieve normal glucose levels. Some of these function by increasing your body's sensitivity to insulin.

Blount says. If your condition progresses to diabetes, you may experience the following symptoms. You should see your doctor right away if you have these symptoms:. Even small changes can have a large impact in delaying or preventing the progression to diabetes.

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Breadcrumb Home Advancing Health Conditions and Services Body Systems Diabetes The difference between insulin resistance and prediabetes. Conditions and Services Body Systems Diabetes The difference between insulin resistance and prediabetes.

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5 Steps to Lower HbA1c Fast! (Insulin Resistance and Diabetes)

HbAc role in insulin resistance -

International Expert Committee International Expert committee report on the role of the A1C assay in the diagnosis of diabetes. Jeon JY, Ko SH, Kwon HS, Kim NH, Kim JH, Kim CS, Song KH, Won JC, Lim S, Choi SH, Jang MJ, Kim Y, Oh K, Kim DJ, Cha BY, Taskforce Team of Diabetes Fact Sheet of the Korean Diabetes A Prevalence of diabetes and prediabetes according to fasting plasma glucose and HbA1c.

Karhapaa P, Voutilainen E, Kovanen PT, Laakso M Insulin resistance in familial and nonfamilial hypercholesterolemia. Arterioscleresis and Thrombosis — Article CAS Google Scholar.

Klein R, Klein BE, Moss SE, Davis MD, DeMets DL Glycosylated hemoglobin predicts the incidence and progression of diabetic retinopathy. J Am Med Assoc — Laakso M, Pyorala K, Voutilainen E, Marniemi J Plasma insulin and serum lipids and lipoproteins in middle-aged non- insulin dependent diabetic and non-diabetic subjects.

Am J Epidemiol — Lee JM, Okumura MJ, Davis MM, Herman WH, Gurney JG Prevalence and determinants of insulin resistance among US adolescents: a population based study.

Article PubMed Google Scholar. Cardiovasc Diabetol —9. Marcovina S, Bowsher RR, Miller WG, Staten M, Myers G, Caudill SP, Campbell SE, Steffes MW Standardization of insulin immunoassays: report of the American Diabetes Association workgroup.

Matsuda M, DeFronzo RA Insulin sensitivity indices obtained from oral glucose tolerance testing. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man.

McLaughlin T, Abbasi F, Cheal K, Chu J, Lamendola C, Reaven GM Use of metabolic markers to identify overweight individuals who are insulin resistant. Ann Intern Med — McLaughlin T, Reaven GM, Abbasi F, Lamendola C, Saad M, Waters D, Simon J, Krauss RM Is there a simple way to identify insulin resistant individuals at increased risk of cardiovascular disease?

Am J Cardiol — Moran A, Jacobs DR, Steinberger J, Hong CP, Prineas R, Luepker R, Sinaiko AR Insulin resistance during puberty: results from clamp studies in children. Moro E, Gallina P, Pais M, Cazzolato G, Alessandrini P, Bittolo-Bon Govindarajalu S Hypertriglyceridemia is associated with increased insulin resistance in subjects with normal glucose tolerance: evaluation in a large cohort of subjects assessed with the World Health Organization criteria for the classification of diabetes.

Metabolism — Perkovic V, Verdon C, Ninomiya T, Barzi F, Cass A, Patel A, Jardine M, Gallagher M, Turnbull F, Chalmers J, Craig J, Huxley R The relationship between proteinuria and coronary risk: a systematic review and meta-analysis. PLoS Med 5:e Article PubMed PubMed Central Google Scholar.

Reaven GM Role of insulin resistance in human disease. Satchell SC, Tooke JE What is the mechanism of microalbuminuria in diabetes: a role for the glomerular endothelium? Simental-Mendia LE, Rodriguez-Moran M, Guerrero-Romero F The product of fasting glucose and triglycerides as surrogate for identifying insulin resistance in apparently healthy subjects.

Metab Syndr Relat Disord — Tapp RJ, Shaw JE, Zimmet PZ, Balkau B, Chadban SJ, Tonkin AM, Welborn TA, Atkins RC Albuminuria is evident in the early stages of diabetes onset: results from the Australian diabetes, obesity, and lifestyle study AusDiab.

American Journal of Kidney Diseases. The official journal of the National Kidney Foundation — Tuomilehto J, Lindstrom J, Eriksson JG, Valle TT, Hamalainen H, Ilanne-Parikka P, Keinanen-Kiukaanniemi S, Laakso M, Louheranta A, Rastas M, Salminen V, Uusitupa M, Finnish Diabetes Prevention Study G: Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance.

The New England Journal of Medicine; — Yeni-Komshian H, Carantoni M, Abbasi F, Reaven GM Relationship between several surrogate estimates of insulin resistance and quantification of insulin-mediated glucose disposal in healthy nondiabetic volunteers.

Ziemer DC, Kolm P, Weintraub WS, Vaccarino V, Rhee MK, Twombly JG, Narayan KM, Koch DD, Phillips LS Glucose-independent, black-white differences in hemoglobin A1c levels: a cross-sectional analysis of 2 studies. Download references. Department of Medicine III, University Hospital Carl Gustav Carus at the TU Dresden, Dresden, Germany.

Department for Prevention and Care of Diabetes, Medical Clinic III, University Clinic Carl Gustav Carus at the Technical University Dresden, Fetscherstraße 74, , Dresden, Germany. You can also search for this author in PubMed Google Scholar.

Correspondence to Peter E. All procedures performed in studies involving human participants were in accordance with the ethical standards of the institution, the Technical University of Dresden. Written informed consent was obtained from all individuals according to the guidelines of the Institutional Review Board for Human Studies at the Technical University of Dresden.

The aim of this study was to investigate the role of HbA1c in predicting insulin resistance among apparently healthy individuals. The study shows that HbA1c has a significant association with insulin resistance markers among young IGT individuals.

The ROC curve also demonstrates that HbA1c occupied a significant area under the curve 0. Reprints and permissions. Saha, S. Impact of glycated hemoglobin HbA1c on identifying insulin resistance among apparently healthy individuals. J Public Health 25 , — Download citation.

Received : 03 June Accepted : 10 April Published : 08 May Issue Date : October Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article.

Provided by the Springer Nature SharedIt content-sharing initiative. Abstract Aims Insulin resistance has been implicated as a risk factor for metabolic disorders. Access this article Log in via an institution. References American Diabetes Association Diagnosis and classification of diabetes mellitus.

Diabetes Care 30 suppl 1 :S42—S47 Article Google Scholar American Diabetes Association Diagnosis and classification of diabetes mellitus. Diabetes Care 33 suppl 1 :S62—S69 Article PubMed Central Google Scholar Bergman RN, Phillips LS, Cobelli C Physiologic evaluation of factors controlling glucose tolerance in man: measurement of insulin sensitivity and beta-cell glucose sensitivity from the response to intravenous glucose.

J Clin Invest — Article CAS PubMed PubMed Central Google Scholar Bonora E, Calcaterra F, Lombardi S, Bonfante N, Formentini G, Bonadonna RC, Muggeo M Plasma glucose levels throughout the day and HbA 1c interrelationships in type 2 diabetes: implications for treatment and monitoring of metabolic control.

Diabetes Care — Article CAS PubMed Google Scholar Brehm A, Pfeiler G, Pacini G, Vierhapper H, Roden M Relationship between serumlipoprotein ratios and insulin resistance in obesity. Clin Chem — Article CAS PubMed Google Scholar Carson AP, Reynolds K, Fonseca VA, Muntner P Comparison of A1C and fasting glucose criteria to diagnose diabetes among US adults.

Diabetes Care —97 Article CAS PubMed Google Scholar Cavaghan MK, Ehrmann DA, Polonsky KS Interactions between insulin resistance and insulin secretion in the development of glucose intolerance. J Clin Invest — Article CAS PubMed PubMed Central Google Scholar DeFronzo RA Lilly lecture.

Diabetes — Article CAS PubMed Google Scholar DeFronzo RA, Tobin JD, Andres R Glucose clamp technique: a method for quantifying insulin secretion and resistance.

Am J Physiol E—E CAS PubMed Google Scholar Ferrannini E, Buzzigoli G, Bonadonna R, Giorico MA, Oleggini M, Graziadei L, Pedrinelli R, Brandi L, Bevilacqua S Insulin resistance in essential hypertension.

N Engl J Med — Article CAS PubMed Google Scholar Ferrara CM, Goldberg AP Limited value of the homeostasis model assessment to predict insulin resistance in older men with impaired glucose tolerance. Diabetes Care — Article CAS PubMed Google Scholar Grundy SM Pre-diabetes, metabolic syndrome, and cardiovascular risk.

J Am Coll Cardiol — Article CAS PubMed Google Scholar Gulli G, Ferrannini E, Stern M, Haffner S, DeFronzo RA The metabolic profile of NIDDM is fully established in glucose-tolerant offspring of two Mexican-American NIDDM parents.

Diabetes — Article CAS PubMed Google Scholar Herman WH, Ma Y, Uwaifo G, Haffner S, Kahn SE, Horton ES, Lachin JM, Montez MG, Brenneman T, Barrett-Connor E, Diabetes Prevention Program Research G Differences in A1C by race and ethnicity among patients with impaired glucose tolerance in the diabetes prevention program.

on the CAROLINA cognition substudy. No other potential conflicts of interest relevant to this article were reported. Author Contributions. performed the analyses and prepared the first draft and subsequent versions. developed the research protocol.

developed the statistical analysis plan with input from M. checked all analyses performed by J. All authors read and approved the final manuscript. is the guarantor of this work and, as such, had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

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Written by Aisling Moran BSc Hons. HbAc role in insulin resistance is a insu,in that helps control Rewistance blood sugar reisstance. This can lead to Chia seed dressings number roke diseases, particularly diabetes. Being overweight and carrying a lot of belly fat are the main risk factors for developing insulin resistance. An HbA1C blood test can check to see if you have this condition. If you do, there are a lot of lifestyle factors that can help reduce or reverse it.

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