Search Menu. Images bloos processed using Alice Software Sugar metabolism Systems, Inc. Type 2 diabetes is the most common form of diabetes, accounting for around

Visceral fat and blood sugar levels -

Older studies have shown that local inflammation in the adipose tissue leads to cardiometabolic abnormalities such as insulin resistance. Now, researchers at Columbia University Irving Medical Center in New York City, NY, help to shed some much-needed light on the issue; they reveal that the liver contributes to this inflammation.

The team was led by Dr. Ira Tabas — who is the Richard J. Stock Professor of Medicine at Columbia University Vagelos College of Physicians and Surgeons — and the findings were published in the journal Nature.

Tabas and his colleagues used obese mice to test whether blocking an enzyme called DPP4 would lower the inflammation in their abdominal fat. The researchers focused on DPP4 because humans who already have diabetes are prescribed DPP4 inhibitors to help them manage their symptoms.

DPP4 inhibitors work by preventing the enzyme from interacting with an insulin-boosting hormone. In this study, DPP4 did not lower abdominal inflammation in mice. Tabas explains these findings, suggesting that they may be down to the difference between how DPP4 inhibitors work in the gut versus how they work in the liver.

If we could block that interaction, we might be able stop the enzyme from causing inflammation and insulin resistance. So, the researchers targeted DPP4 in the liver cells instead of the gut. This reduced adipose inflammation and lowered insulin resistance.

As Dr. The researchers explain what the findings mean for future treatments of type 2 diabetes. Ahmed A.

More research is needed. In this article, we look at nine ways to lower high insulin levels. This can be achieved through diet, lifestyle changes, supplements, and medication.

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Medical News Today. 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. 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. Advanced Search. User Tools Dropdown. Sign In. Skip Nav Destination Close navigation menu Article navigation. Volume 51, Issue Previous Article Next Article. RESEARCH DESIGN AND METHODS.

Article Information. Article Navigation. Obesity Studies October 01 Removal of Visceral Fat Prevents Insulin Resistance and Glucose Intolerance of Aging : An Adipokine-Mediated Process? Ilan Gabriely ; Ilan Gabriely. This Site. Google Scholar. Xiao Hui Ma ; Xiao Hui Ma. Xiao Man Yang ; Xiao Man Yang.

Gil Atzmon ; Gil Atzmon. Michael W. Rajala ; Michael W. Anders H. Berg ; Anders H. Phillip Scherer ; Phillip Scherer. Luciano Rossetti ; Luciano Rossetti. Nir Barzilai Nir Barzilai. Diabetes ;51 10 — Get Permissions. toolbar search Search Dropdown Menu.

toolbar search search input Search input auto suggest. View large Download slide. TABLE 1 Body composition and fat distribution of aging rats. young and CR;. All data are presented as means ± SE.

View Large. TABLE 2 Metabolic characteristics of aging rats. TABLE 3 Body composition and fat distribution of ZDF rats. TABLE 4 Metabolic characteristics of ZDF rats. Cefalu WT, Wang ZQ, Werbel S, Bell-Farrow A, Crouse JR 3rd, Hinson WH, Terry JG, Anderson R: Contribution of visceral fat mass to the insulin resistance of aging.

Shimokata H, Tobin JD, Muller DC, Elahi D, Coon PJ, Andres R: Studies in the distribution of body fat. Effects of age, sex, and obesity. J Gerontol. Ferrannini E, Natali A, Capaldo B, Lehtovirta M, Jacob S, Yki-Jarvinen H: Insulin resistance, hyperinsulinemia, and blood pressure: role of age and obesity: European Group for the Study of Insulin Resistance EGIR.

Fujimoto WY, Bergstrom RW, Boyko EJ, Chen KW, Leonetti DL, Newell-Morris L, Shofer JB, Wahl PW: Visceral adiposity and incident coronary heart disease in Japanese-American men: the year follow-up results of the Seattle Japanese-American Community Diabetes Study.

Diabetes Care. Lamarche B: Abdominal obesity and its metabolic complications: implications for the risk of ischaemic heart disease. Coron Artery Dis. Carey DG, Jenkins AB, Campbell LV, Freund J, Chisholm DJ: Abdominal fat and insulin resistance in normal and overweight women: direct measurements reveal a strong relationship in subjects at both low and high risk of NIDDM.

Williamson JR, Kreisberg RA, Felts PW: Mechanism for the stimulation of gluconeogenesis by fatty acids in perfused rat liver. Proc Natl Acad Sci U S A. Steppan CM, Bailey ST, Bhat S, Brown EJ, Banerjee RR, Wright CM, Patel HR, Ahima RS, Lazar MA: The hormone resistin links obesity to diabetes.

Hotamisligil GS, Peraldi P, Budavari A, Ellis R, White MF, Spiegelman BM: IRSmediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance.

Barzilai N, Banerjee S, Hawkins M, Chen W, Rossetti L: Caloric restriction reverses hepatic insulin resistance in aging rats by decreasing visceral fat. J Clin Invest. Masoro EJ: Possible mechanisms underlying the antiaging actions of caloric restriction. Toxicol Pathol. Barzilai N, She L, Liu BQ, Vuguin P, Cohen P, Wang J, Rossetti L: Surgical removal of visceral fat reverses hepatic insulin resistance.

Barzilai N, Hawkins M, Angelov I, Hu M, Rossetti L: Glucosamine-induced inhibition of liver glucokinase impairs the ability of hyperglycemia to suppress endogenous glucose production.

Hawkins M, Barzilai N, Liu R, Hu M, Chen W, Rossetti L: Role of the glucosamine pathway in fat-induced insulin resistance. Barzilai N, Rossetti L: Relationship between changes in body composition and insulin responsiveness in models of the aging rat.

Am J Physiol.

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