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Visceral fat and insulin sensitivity

Visceral fat and insulin sensitivity

High-intensity workouts The inslin of anthropometric waist circumference and Cholesterol-lowering yogurt blood pressure sebsitivity with abnormalities in glucose and lipid Cholesterol-lowering yogurt has Visceral fat and insulin sensitivity motivation for iinsulin lot of discussions in the last 30 years. Kreier F, Fliers E, Voshol PJ, Eden CGV, Havekes LM, Kalsbeek A, et al. Here, we used the Zucker Fatty rat model, which resembles common features of obese patients developing type 1 diabetes Ele Ferrannini. On the basis of earlier findings 20assessment of the cerebrocortical insulin effect as changes in theta activity during the insulin experiment corrected for the placebo experiment were calculated

Visceral fat and insulin sensitivity -

In both groups, the removal of the abdominal subcutaneous fat had no effect on insulin resistance, plasma glucose or insulin levels, plasma adiponectin levels, or any of the lipid or inflammatory components of the metabolic syndrome. Pioglitazone, rosiglitazone, and troglitazone have been shown to increase total body fat and abdominal subcutaneous adipose tissue while having no effect on or slightly decreasing visceral adipose tissue.

Despite this increase in overall obesity, the thiazolidinediones improve insulin sensitivity and improve all of the components of the metabolic syndrome This sequence of events suggests that insulin resistance and the components of the metabolic syndrome are the consequence of the metabolic effects of the products being released from the adipose tissue rather than an effect of the absolute mass of the tissue.

Adipose tissue releases free fatty acids and cytokines e. It is the net effect of these factors that appears to be responsible for the metabolic abnormalities of obesity.

We have presented evidence that we believe supports the thesis that increases in visceral adipose tissue are the conduit by which obesity leads to insulin resistance and the metabolic syndrome. Further validation requires many additional pieces of the puzzle to be unraveled and explained.

Visceral adipose tissue is biochemically quite distinct from subcutaneous adipose tissue, as has been reviewed by several authors 30 , and it is unclear as to how the large number of adipokines, cytokines, and enzymes as diverse as adiponectin and 11β-hydroxysteroid dehydrogenase type 1 are regulated and integrated.

Several recent studies involving nondiabetic Asian Indians suggest that regional adipose tissue metabolic activity may be quantitatively different depending on the ethnic background of the individual. For the same fat mass and regional distribution, Asian Indians have more insulin resistance, higher plasma free fatty acids, higher C-reactive protein and plasminogen activator inhibitor-1, and lower plasma adiponectin than Caucasians The relationship between visceral adipose tissue and abdominal subcutaneous tissue may be more closely linked than has been thought.

There are a few studies suggesting that increases in visceral adipose tissue mass or activity may alter subcutaneous adipose cell lipolysis. It has become increasingly evident that the effects of visceral adiposity must be mediated by multiple factors.

As Klein 32 has commented in a recent editorial, it is unlikely that the contribution that visceral fat makes to the free fatty acid flux in the circulation is its major mechanism in causing insulin resistance.

Sign In or Create an Account. Search Dropdown Menu. header search search input Search input auto suggest. filter your search All Content All Journals Diabetes Care.

Advanced Search. User Tools Dropdown. Sign In. Skip Nav Destination Close navigation menu Article navigation. Volume 28, Issue 9. Previous Article Next Article. Correlation between adipose tissue depots and insulin resistance.

Absence of insulin resistance in overweight and obese individuals with lower body obesity. Adipose tissue composition and metabolic status in patients with the Prader-Willi syndrome.

Liposuction removal of abdominal subcutaneous adipose tissue in obese nondiabetic and type 2 diabetic subjects. Peroxisome proliferator—activated receptor γ agonists increase abdominal subcutaneous adipose tissue mass but decrease insulin resistance and improve most of the components of the metabolic syndrome.

Article Navigation. Editorials September 01 Point: Visceral Adiposity Is Causally Related to Insulin Resistance Harold E. Lebovitz, MD ; Harold E. Lebovitz, MD. From the Division of Endocrinology, Department of Medicine, State University of New York Health Science Center at Brooklyn, Brooklyn, New York.

This Site. Google Scholar. Mary Ann Banerji, MD, FACP Mary Ann Banerji, MD, FACP. Although plasma insulin levels were higher than during the basal period, it should be pointed out that insulin was infused peripherally during the pancreatic clamp procedure.

Indeed, resistance to the inhibitory action of insulin on EGP was also present in the face of hyperglycemia, which may have an independent effect on decreasing EGP. However, all animals became diabetic when most of the VF regenerated Fig.

The expression of leptin and TNF-α were estimated in VF and SC fat. CR rats had plasma leptin levels 3. Prevention treatment strategies have been successfully applied to type 2 diabetes. Lifestyle modifications largely designed to alter fat mass and distribution are the cornerstone of these interventions and have been shown to delay the onset of hyperglycemia in individuals at high risk for the disease 20 , Similarly, chronic CR has dramatic beneficial effects on glucose tolerance and insulin action in rodents 12 and in primates Importantly, reduction in visceral adiposity is a common feature of all these interventions.

However, it has been difficult to discern whether a reduction in the size of intra-abdominal fat depots plays a causative role or is simply a covariant tightly associated with one or more causative factors. Here, we show that surgical removal of two intra-abdominal fat depots prevents the onset of age-dependent insulin resistance and markedly delays the onset of glucose intolerance and diabetes in a rodent model of obesity and diabetes.

Our findings indicate that a modest decrease in total fat mass per se does not have a significant impact on insulin action.

However, not all fat depots have equal metabolic import. Adipose tissue from different anatomical sites has markedly different effects on metabolic outcomes. In fact, removal of a similar amount of adipose tissue from the peri-renal and peri-epididymal sites VF led to dramatic improvements in peripheral and hepatic insulin sensitivity and glucose tolerance.

The onset of diabetes in the ZDF rats tracked very closely with the regeneration of VF several weeks after its surgical removal. Our results may provide useful information in the contentious debate regarding the mechanism s by which CR improves metabolic parameters and extends life in rodent models Until recently, the effects of CR on life extension 24 , 25 were related directly to the decreased intake of nutrients rather than to secondary effects on body weight, fat mass, or distribution of body fat.

This study documents that insulin action can be improved in the absence of CR, challenging the notion that nutrient excess per se is the prominent cause of insulin resistance in this aging model.

Overall, the dramatic improvement in peripheral and hepatic insulin action after removal of visceral but not SC adipose tissue resembles the effects of prolonged CR in aging rodents However, a closer look at other associated variables in the two intervention models also reveals striking differences.

CR results in marked reductions in body weight, total fat mass, and lean body mass. Conversely, the surgical removal of VF markedly improves metabolic parameters in the absence of any detectable changes in body weight, fat mass, and lean body mass. Furthermore, the reduction in VF is the result of a proportional decrease in all VF depots with CR, whereas it is entirely due to decreased epididymal and perinephric fat in our surgical model.

Thus, decreased VF could largely account for the beneficial metabolic effects of chronic CR. However, our results cannot quantify the relative contribution of mesenteric, epididymal, and perinepric fat depots in mediating these effects.

Insulin resistance is a major risk factor for the development of diabetes in humans and animals Here, we used the Zucker Fatty rat model, which resembles common features of obese patients developing type 1 diabetes This model is characterized by marked hyperinsulinemia and insulin resistance Thus, removal of VF dramatically improved insulin sensitivity in Zucker Fatty rats.

Thus, selective intra-abdominal fat depots play a major role in modulating insulin action and glucose tolerance in these two animal models. Can we speculate on potential mechanism s by which these depots regulate insulin action in distant sites?

One possibility is that increased plasma levels of FFAs and glycerol impair insulin action in both the liver and muscle 29 — In fact, it has been suggested that VF is resistant to the antilipolytic effects of insulin, and its removal may have decreased the flux of FFAs and glycerol to these target organs However, the concentrations of FFAs and glycerol were unchanged in these experimental models at both basal conditions and during the studies.

It should also be pointed out that the venous drainage of the mesenteric fat is portal, whereas that of the epididymal and perinephric fat is caval.

Recent evidence indicates that adipose cells are also capable of biosynthesis and secretion of several metabolically active factors Some of these factors circulate in plasma and are active at distant targets 19 , In this regard, it is of interest that the mRNA encoding for the novel circulating protein resistin was much higher in epididymal and perinephric adipose tissue than in SC adipose tissue.

The extraction of VF also resulted in marked changes in the expression of the fat-derived peptide TNF-α in the SC adipose tissue. TNF-α may be directly involved in the development of insulin resistance in obesity through its effects on insulin signaling VF removal was also associated with decreased plasma concentrations of both insulin and leptin.

Leptin mRNA in SC adipose tissue was also decreased. The decline in circulating levels of these hormones may simply reflect their improved biological action. However, it is also likely that a decrease in plasma insulin concentrations and perhaps decreased carbon flux into the hexosamine pathway may account for the decreased expression of leptin in SC adipose tissue after VF removal Finally, removal of VF resulted in a significant decrease in plasma Acrp30 levels.

Thus, because Acrp30 normally induces a potentiation of insulin action, the improvements in systemic insulin sensitivity seen with VF removal was probably mediated through mechanisms distinct from an increase in circulating Acrp30 levels.

Our results indicate that the surgical removal of selective intra-abdominal fat depots prevents the age-related decrease in peripheral and hepatic insulin action and may regulate gene expression in SC adipose tissue.

Furthermore, removal of VF delays the onset of diabetes in the ZDF model of obesity and diabetes. Thus, we propose that specific interventions designed to reduce intra-abdominal adiposity will greatly improve insulin action.

Further studies will be necessary to identify the specific fat-derived signals by which selective depots of adipose tissue regulates glucose fluxes and gene expression at distant sites.

Peripheral insulin sensitivity in aging rats. Shown are results for young 2-month-old and old month-old F1 hybrids of F and Brown Norway rats. Hepatic insulin sensitivity in aging rats. The ability of insulin to suppress EGP was studied using glucose tracer methodology see research design and methods.

R a , rate of EGP. Development of diabetes and the regrowth of VF in ZDF rats. Six rats from each group were studied using a pancreatic clamp, and the rest were monitored for 4 months until they developed diabetes. Gene expression of TNF-α and leptin.

RT and real-time PCR analysis for TNF-α, leptin, and β-actin are described in research design and methods. B : Analysis of all real-time PCR data obtained in all rats, corrected for intensity of β-actin and presented in arbitrary units.

mesenteric fat. Gene expression of resistin A and ACRP30 B. B : Real-time PCR data obtained from all rats corrected for the intensity of β-actin and presented in arbitrary units.

M and SC. young 2-month-old , and old month-old F1 hybrids of F and Brown Norway rats were used in these experiments. The table depicts the amounts of VF or SC removed at the surgery, body weight, lean body mass, non-VF fat mass, total VF, and epididymal, perinephric, and mesenteric fat, which were determined at killing after the experiments.

Plasma glucose, insulin, FFA concentrations, basal rate of EGP R a , glucose infusion rate GIR , glycolysis Gly , and glycogen synthesis GS during the basal period and during the pancreatic euglycemic clamp are shown.

These parameters were measured at basal conditions and during the insulin clamps see group description in research design and methods. The table depicts the amounts of VF removed at surgery, body weight, lean body mass, non-VF fat mass, and total VF, epididymal, perinephric, and mesenteric fat that were detected after the study.

This work was supported by grants from the National Institutes of Health Paul Beeson Physician Faculty Scholar in Aging Award and RO1-AG to N. and RDK and ROI-DK to L.

Address correspondence and reprint requests to Nir Barzilai, Institute for Aging Research, Belfer Bldg. E-mail: barzilai aecom.

CR, caloric restriction; dsDNA, double-stranded DNA; EGP, endogenous glucose production; FFA, free fatty acid; SC, subcutaneous; TNF-α, tumor necrosis factor-α; VF, visceral fat.

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Advanced Search. User Tools Dropdown. Sign In. Skip Nav Destination Close navigation menu Article navigation. Volume 51, Issue Previous Article Next Article.

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Visceral fat and insulin sensitivity Gastaldelli, Viscrral Miyazaki, Maura Pettiti, Masafumi Sensitivitt, Srihanth Mahankali, Eleonora Santini, Ralph A. Visceral fat VF excess has been Visceral fat and insulin sensitivity Grape Sorbet Recipe Ideas decreased peripheral insulin sensitivity and Visceral fat and insulin sensitivity senxitivity suggested to contribute to hepatic insulin resistance. However, iVsceral mechanisms by which Fatt impacts on hepatic glucose metabolism and the quantitative role of VF in glycemic control have not been investigated. In the present study 63 type 2 diabetic subjects age, 55 ± 1 yr; fasting plasma glucose, 5. In contrast, the relation of basal endogenous glucose output to VF was not statistically significant. We conclude that in patients with established type 2 diabetes, VF accumulation has a significant negative impact on glycemic control through a decrease in peripheral insulin sensitivity and an enhancement of gluconeogenesis.

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