EFFECTS OF INSULIN SENSITIZERS AND PPAR LIGANDS ON LIPOTOXICITY IN SUBJECTS WITH

胰岛素增敏剂和 PPAR 配体对患有以下疾病的受试者的脂毒性的影响

• 批准号: 7377692
• 负责人: Neda Rasouli
• 金额: $ 1万
• 依托单位: UNIV OF ARKANSAS FOR MED SCIS
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-04-01 至 2007-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7377692
• 关键词: EFFECTS; INSULIN; SENSITIZERS; PPAR; LIGANDS

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 is associated with insulin resistance and increased lipid accumulation in skeletal muscle, pancreas, and liver, with resulting functional impairment that has been called lipotoxicity. The factors leading to ectopic lipid accumulation and the best intervention to reverse this pathophysiology are not clear. We will examine insulin sensitivity, intramyocellular fat content, adipokines secretion and changed in the pattern of gene expression in subjects with impaired glucose tolerance in response to different PPAR ligands. We propose that PPAR a ligand (fenofibrate) and PPAR ? ligand (pioglitazone) will reduce muscle lipid accumulation by stimulating muscle lipid oxidation and redistribution of lipid from muscle to adipocytes respectively. The combination of both medications will be particularly effective at reducing muscle lipid accumulation. These studies are designed to examine fundamental clinical mechanisms underlying the metabolic syndrome and diabetes.

该子项目是利用 NIH/NCRR 资助的中心拨款提供的资源的众多研究子项目之一。子项目和研究者 (PI) 可能已从另一个 NIH 来源获得主要资金，因此可以在其他 CRISP 条目中得到体现。列出的机构是中心的机构，不一定是研究者的机构。肥胖与胰岛素抵抗和骨骼肌、胰腺和肝脏中脂质积累增加有关，从而导致功能障碍，称为脂毒性。导致异位脂质积累的因素以及扭转这种病理生理学的最佳干预措施尚不清楚。我们将检查糖耐量受损受试者对不同 PPAR 配体的反应中的胰岛素敏感性、肌细胞内脂肪含量、脂肪因子分泌以及基因表达模式的变化。我们建议 PPAR 配体（非诺贝特）和 PPAR ？配体（吡格列酮）将分别通过刺激肌肉脂质氧化和脂质从肌肉到脂肪细胞的重新分配来减少肌肉脂质积累。两种药物的组合对于减少肌肉脂质积累特别有效。这些研究旨在检查代谢综合征和糖尿病的基本临床机制。