Prednisolone Altered Chromium Distribution in Diet-Induced Obesity Mice

• Main Authors: ChungDe Chen, 陳宗德
• Other Authors: Frank Chiahung Mao
• Format: Others
• Language: zh-TW
• Published: 2005
• Online Access: http://ndltd.ncl.edu.tw/handle/95086172194622132620

碩士 === 國立中興大學 === 獸醫學系 === 93 === Obesity is a major risk factor for the development of insulin resistance, type 2 diabetes mellitus (DM) and coronary heart disease. It is now clear that obesity promotes the development of metabolic syndrome (Syndrome X) and type 2 DM. In clinical medical studies of human and experimental animals, long-term use of glucocorticoids could lead to symptoms of the metabolic syndrome, including obesity, insulin resistance, glucose intolerance and hyperglycemia. Trivalent chromium has proven to be a cofactor for insulin action, it facilitates the movement of glucose into cells, enhances insulin binding to insulin receptors, and improves glucose disposal for prevention of type 2 DM. Based on animal and preliminary human studies, steroid-induced diabetes can be reversed by chromium supplementation. In 2004, Coldfelder et al indicated that the transportation and distribution of chromium were altered in response to the increases serum glucose or insulin in both normal and diabetic mice however, the mechanisms of chromium transportation are still unknown. Here, we used diet-induced obesity (DIO) model to mimic human obesity in C57BL/6J male mice. C57BL/6J male mice were divided into normal chow diet and high-fat diet groups and fed for 12 weeks before the body chromium distribution and abnormality in energy metabolism were compared. Our second study was to investigate body chromium distribution, insulin resistance index (HOMA-IR), fasting serum glucose level, fasting serum triglyceride level as well as serum insulin and leptin levels 24hrs after a bolus intraperitoneal injection (2mg/kg) of prednisolone to obese C57BL/6J mice with metabolic syndrome and KK/HlJ type 2 diabetic mice. The results indicated a successful induction of metabolic syndrome by DIO model, promoting hypertriglyceridemia, hyperglycemia, hyperinsulinemia and obesity in C57BL/6J and KK/HlJ mice. Single dose of prednisolone significantly decreased chromium concentration in insulin-sensitive tissues such as liver, fat and skeletal muscle but chromium concentration in femoral bone was significantly increased; which lead to abnormality of glucose/lipid metabolism. This alteration of chromium distribution and glucose metabolism was especially prominent in high-fat diet group. In conclusion, the study strongly suggested that obesity could enhance the movement of chromium distribution induced by a bolus dose of 2 mg/kg of prednisolone which ultimately lead to abnormal glucose and lipid metabolism.