Surgical removal of visceral adipose tissue: Effects on insulin action
Rent the article at a discountRent now
* Final gross prices may vary according to local VAT.Get Access
Many studies have demonstrated that excess of visceral fat has deleterious effects on insulin action. Mainly, it has been shown to be associated with a decrease in hepatic and peripheral insulin sensitivity, which results in a clinical condition also known as insulin resistance. This report describes a novel experimental method that we employed in order to analyze the particular effects of visceral fat on insulin activity. By extracting visceral fat we were able to distinguish the specific role that it plays in insulin action, and to analyze its effects on the gene expression of a variety of fat-derived peptides, which may be considered to be (at least partially) mediators in the development of the metabolic syndrome and possibly diabetes mellitus.
- Peiris AN, Struve MF, Mueller RA, et al.: Glucose metabolism in obesity: influence of body fat distribution. J Clin Endocrinol Metab 1988, 67:760–767. CrossRef
- Carey DG, Jenkins AB, Campbell LV, et al.: 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. Diabetes 1996, 45:633–638. CrossRef
- O'Shaughnessy IM, Myers TJ, Stepniakowski K, et al.: Glucose metabolism in abdominally obese hypertensive and normotensive subjects. Hypertension 1995, 26:186–192.
- Bjorntorp P: "Portal" adipose tissue as a generator of risk factors for cardiovascular disease and diabetes. Arteriosclerosis 1990, 10:493–496.
- Argaud D, Zhang Q, Pan W, et al.: Regulation of rat liver glucose-6-phosphatase gene expression in different nutritional and hormonal states: gene structure and 5′-flanking sequence. Diabetes 1996, 405:1563–1571. CrossRef
- Gabbay RA, Sutherland C, Gnudi L, et al.: Insulin regulation of phosphoenolpyruvate carboxykinase gene expression does not require activation of the Ras/mitogen-activated protein kinase. J Biol Chem 1996, 271:1890–1897. CrossRef
- O'Brien RM, Noisin EL, Suwanichkul A, et al.: Hepatic nuclear factor 3- and hormone-regulated expression of the phosphoenolpyruvate carboxykinase and insulin-like growth factorbinding protein 1 genes. Mol Cell Biol 1995, 15:1747–1758.
- Barzilai N, Banerjee S, Hawkins M, et al.: Caloric restriction reverses hepatic insulin resistance in aging rats by decreasing visceral fat. J Clin Invest 1998, 101:1353–1361.
- Barzilai N, Hawkins M, Massilon D, et al.: Leptin selectively decreases visceral adiposity and enhances peripheral and hepatic insulin action. J Clin Invest 1997, 100:3105–3110.
- Barzilai N, She L, Liu BQ, et al.: Surgical removal of visceral fat reverses hepatic insulin resistance. Diabetes 1999, 48:94–98. Describes a novel experimental paradigm used to examine the specific effects of VF on hepatic insulin resistance. Specifically removing VF induced a significant improvement in hepatic insulin sensitivity. This improvement was associated with an approximately 70% decrease in plasma levels of IGFBP-1, a marker of insulin's transcription regulation in the liver, and marked decreases in the gene expression of TNF-α and leptin in SC fat. CrossRef
- Barzilai N, Gabriely I: The role of fat depletion in the biological benefits of caloric restriction. J Nutr 2001, 131:903S-906S.
- Masoro EJ: Possible mechanisms underlying the antiaging actions of caloric restriction. Toxicol Pathol 1996, 24:738–741.
- Masoro EJ: Caloric restriction and aging: an update. Exp Gerontol 2000, 35:299–305. CrossRef
- Weindruch R: The retardation of aging by caloric restriction: studies in rodents and primates. Toxicol Pathol 1996, 24:742–745. CrossRef
- Gabriely I, MaXH, YangXM, et al.: Removal of visceral fat prevents insulin resistance and glucose intolerance of aging: an adipokine-mediated process? Diabetes 2002, 51:2951–2958. Demonstrates the extraction of VF in old rats is sufficient to restore peripheral and hepatic insulin action to the levels of young rats. When examined at the mechanistic level, removal of VF in Zucker Diabetic Fatty rats prevented the progressive decrease in insulin action and delayed the onset of diabetes. Taken together, these data suggest that VF plays a pivotal role not only in the modulation of insulin sensitivity (hepatic and peripheral) associated with aging, but also in delaying the onset and progression of diabetes. CrossRef
- Wagner R, Oberste-Berghaus C, Herpertz S, et al.: Time relationship between circadian variation of serum levels of leptin, insulin and cortisol in healthy subjects. Horm Res 2000, 54:174–180. CrossRef
- Rossetti L, Hawkins M, Chen W, et al.: In vivo glucosamine infusion induces insulin resistance in normoglycemic but not in hyperglycemic conscious rats. J Clin Invest 1995, 96:132–140.
- Wang J, Liu R, Hawkins M, et al.: A nutrient sensing pathway regulates leptin gene expression in muscle and fat. Nature 1998, 393:684–688. Provides evidence for rapid activation of ob gene expression in skeletal muscle by glucosamine. Increased tissue concentrations of the end product of the hexosamine biosynthetic pathway, UDP-N-acetylglucosamine, resulted in rapid and marked increases in leptin mRNA and protein levels. Similarly, plasma leptin levels and leptin mRNA and protein levels in adipose tissue also increased. Most importantly, stimulation of leptin synthesis was shown to be reproduced by either hyperglycemia or hyperlipidemia, which also increase tissue levels of UDP-N-acetylglucosamine. CrossRef
- Gabriely I, Yang XM, Cases JA, et al.: Hyperglycemia induces PAI-1 gene expression in adipose tissue by activation of the hexosamine biosynthetic pathway. Atherosclerosis 2002, 160:115–122. CrossRef
- Barzilai N, Gupta G: Interaction between aging and syndrome X: new insights on the pathophysiology of fat distribution. Ann N Y Acad Sci 1999, 892:58–72. CrossRef
- Wang J, Liu R, Liu L, et al.: The effect of leptin on Lep expression is tissue-specific and nutritionally regulated. Nat Med 1999, 5:895–899. CrossRef
- Hotamisligil GS, Budavari A, Murray D, et al.: Reduced tyrosine kinase activity of the insulin receptor in obesity-diabetes. Central role of tumor necrosis factor-alpha. J Clin Invest 1994, 94:1543–1549.
- Kanety H, Feinstein R, Papa MZ, et al.: Tumor necrosis factor alpha-induced phosphorylation of insulin receptor substrate-1 (IRS-1). Possible mechanism for suppression of insulin-stimulated tyrosine phosphorylation of IRS-1. J Biol Chem 1995, 270:23780–23784. CrossRef
- Hotamisligil GS, Shargill NS, Spiegelman BM: Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance. Science 1993, 259:87–91. CrossRef
- Uysal KT, Wiesbrock SM, Marino MW, et al.: Protection from obesity-induced insulin resistance in mice lacking TNF-alpha function. Nature 1997, 389:610–614. CrossRef
- Hotamisligil GS, Arner P, Caro JF, et al.: Increased adipose tissue expression of tumor necrosis factor-alpha in human obesity and insulin resistance. J Clin Invest 1995, 95:2409–2415. CrossRef
- Hofmann C, Lorenz K, Braithwaite SS, et al.: Altered gene expression for tumor necrosis factor-alpha and its receptors during drug and dietary modulation of insulin resistance. Endocrinology 1994, 134:264–270. CrossRef
- Scherer PE, Williams S, Fogliano M, et al.: A novel serum protein similar to C1q, produced exclusively in adipocytes. J Biol Chem 1995, 270:26746–26749. CrossRef
- Gabriely I, Yang XM, Cases JA, et al.: Hyperglycemia modulates angiotensinogen gene expression. Am J Physiol 2001, 281:R795-R802.
- Steppan CM, Bailey ST, Bhat S, et al.: The hormone resistin links obesity to diabetes. Nature 2001, 409:307–312. CrossRef
- Combs TP, Berg AH, Obici S, et al.: Endogenous glucose production is inhibited by the adipose-derived protein Acrp30. J Clin Invest 2001, 108:1875–1881. CrossRef
- Surgical removal of visceral adipose tissue: Effects on insulin action
Current Diabetes Reports
Volume 3, Issue 3 , pp 201-206
- Cover Date
- Print ISSN
- Online ISSN
- Current Medicine Group
- Additional Links