%0 Journal Article
%T Effects of Acute Exercise and Chronic Exercise on the Liver Leptin-AMPK-ACC Signaling Pathway in Rats with Type 2 Diabetes
%A Xuejie Yi
%A Shicheng Cao
%A Bo Chang
%A Dalin Zhao
%A Haining Gao
%A Yihan Wan
%A Jiaojiao Shi
%A Wei Wei
%A Yifu Guan
%J Journal of Diabetes Research
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/946432
%X Aim. To investigate the effects of acute and chronic exercise on glucose and lipid metabolism in liver of rats with type 2 diabetes caused by a high fat diet and low dose streptozotocin (STZ). Methods. Animals were classified into control (CON), diabetes (DC), diabetic chronic exercise (DCE), and diabetic acute exercise (DAE) groups. Results. Compared to CON, the leptin levels in serum and liver and ACC phosphorylation were significantly higher in DC, but the levels of liver leptin receptor, AMPK¦Á1/2, AMPK¦Á1, and ACC proteins expression and phosphorylation were significantly lower in DC. In addition, the levels of liver glycogen reduced significantly, and the levels of TG and FFA increased significantly in DC compared to CON. Compared to DC, the levels of liver AMPK¦Á1/2, AMPK¦Á2, AMPK¦Á1, and ACC phosphorylation significantly increased in DCE and DAE. However, significant increase of the level of liver leptin receptor and glycogen as well as significant decrease of the level of TG and FFA were observed only in DEC. Conclusion. Our study demonstrated that both acute and chronic exercise indirectly activated the leptin-AMPK-ACC signaling pathway and increased insulin sensitivity in the liver of type 2 diabetic rats. However, only chronic and long-term exercise improved glucose and lipid metabolism of the liver. 1. Introduction Leptin deficiency or dysfunction is one of the main causes for insulin resistance (IR) and lipid metabolism disorders [1, 2]. However, patients with type 2 diabetes rarely have a leptin deficiency. It has been found that the majority of type 2 diabetes patients have higher levels of body fat, but normal or increased leptin in the plasma [3¨C6], indicating leptin resistance (LR). Certain levels of leptin effectively could stimulate AMP-activated protein kinase (AMPK) to phosphorylate acetyl-coA carboxylase (ACC), which in turn reduces the ACC activity, decreases fatty acid synthesis [7], and increases the oxidation of fatty acid (FA) [8], consequently, maintaining the balance of lipid metabolism in the body. Studies have shown that even one week of a high fat diet can cause leptin to increase rapidly, leading to fat accumulation in peripheral tissue IR [9]. Obese persons with high serum leptin levels tend to experience a downregulation of leptin receptor in hypothalamus, adipose tissue, and liver [10], which causes peripheral tissues to become LR and promotes lipid accumulation [11¨C13]. Excessive lipid deposition in nonfat tissue has been known to have a toxic effect on cells and to reduce sensitivity to insulin, eventually leading to
%U http://www.hindawi.com/journals/jdr/2013/946432/