THE ROLE OF INTRAMYOCELLULAR LIPID ACCUMULATION ON THE INSULIN RESISTANCE OF OBE

本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者（PI）可能已经从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。列出的机构是中心的，不一定是研究者的机构。肥胖在过去的一代人中越来越普遍，是一个严重的公共健康问题。肥胖是心血管疾病、中风、某些类型的癌症和2型糖尿病的重要危险因素。肥胖通过胰岛素抵抗导致2型糖尿病。然而，肥胖诱导的胰岛素抵抗的确切机制尚未确定。本研究旨在通过探讨细胞内脂质（IMCL）积累对胰岛素信号级联的影响来阐明可能的机制。该研究是一项前瞻性干预试验，旨在评估减肥对一组健康肥胖成人的IMCL和胰岛素抵抗的影响。本项目将探讨IMCL、瘦素、胰岛素、葡萄糖和血清甘油三酯水平与胰岛素抵抗的相互作用，以及饮食干预计划后这些因素的改善。了解肥胖诱导的胰岛素抵抗机制将有助于2型糖尿病的预防和治疗。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Obesity has been increasing in prevalence the past generation and is a serious public health problem. Obesity is an important risk factor for cardiovascular disease, stroke, some types of cancer, and type 2 diabetes. Obesity leads to type 2 diabetes through insulin resistance. However, the exact mechanism of obesity-induced insulin resistance has not been established. The proposed study aims to elucidate the possible mechanism by exploring the effects of intramyocellular lipid (IMCL) accumulation on the insulin-signaling cascade. The study is a prospective intervention trial to assess the effects of weight loss on the IMCL and insulin resistance of a group of healthy obese adults. This project will explore the interaction of IMCL, leptin, insulin, glucose and serum triglyceride levels on insulin resistance and the improvement of those factors after a dietary intervention program. Understanding the mechanism of obesity-induced insulin resistance will benefit the development of possible prevention and treatment for type 2 diabetes.