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Adipocytokines and the Regulation of Lipid Metabolism in Growth Hormone Transgenic and Calorie-Restricted Mice

Geriatrics Research (Z.W., M.M.M., A.B.), Department of Physiology and Internal Medicine, School of Medicine, Southern Illinois University, Springfield, Illinois 62794-9628; Division of Diabetes, Endocrinology, and Metabolism (Z.W.), School of Medicine, Vanderbilt University, Nashville, Tennessee 37232-6303; and Department of Physiology (K.A.A.-R.), College of Medicine, King Saud University, Riyadh, Saudi Arabia 11461

Address all correspondence and requests for reprints to: Zhihui Wang, M.D., Ph.D., Division of Diabetes, Endocrinology, and Metabolism, School of Medicine, Vanderbilt University, 712 PRB, 2220 Pierce Avenue, Nashville, Tennessee 37232-6303. E-mail: zhihui.wang{at}vanderbilt.edu.

Chronic elevation of GH induces resistance to insulin and hyperinsulinemia in both humans and animals, whereas calorie restriction (CR) improves peripheral insulin sensitivity in many species. To investigate the mechanisms that lead to insulin resistance in animals with high levels of GH as well as the mechanisms that might improve insulin sensitivity, we fed GH-overexpressing transgenic mice ad libitum or subjected them to 30% CR. We then assayed the plasma adipocytokines levels related to insulin sensitivity, plasma lipid levels, and tissue triglycerides accumulation and examined adipocyte morphology. Furthermore, we evaluated mRNA expression and protein levels of enzymes or regulators involved in regulating hepatic lipid metabolism. Our results suggest that decreased plasma adiponectin, increased plasma resistin and cholesterol, and elevated levels of TNF- and IL-6 in adipocytes may all contribute to the insulin resistance observed in GH-Tg mice. Increased accumulation of triglycerides and impaired adipocytes differentiation in GH-transgenic mice provide plausible mechanisms for the alterations of adipocytokines. Hepatic and muscle insulin resistance in these mice is probably related to excessive accumulation of fatty acids and their metabolites. An increase in plasma adiponectin and decrease in plasma IL-6, triglycerides, and cholesterol levels in response to CR may improve insulin sensitivity.

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