Research Progress on Pathogenesis of Obesity-Induced Insulin Resistance and Its Therapeutic Targets: PPARα/γ

被引:1
|
作者
Qi, Zhigang [1 ]
Xie, Meilin [1 ]
机构
[1] Soochow Univ, Coll Med, Dept Pharmacol, Suzhou 215123, Jiangsu, Peoples R China
关键词
obesity; insulin resistance; PPAR alpha/gamma; FATTY-ACID OXIDATION; NF-KAPPA-B; ACTIVATED PROTEIN-KINASE; BETA-CELL DYSFUNCTION; HUMAN SKELETAL-MUSCLE; METABOLIC SYNDROME; ADIPOSE-TISSUE; GLOBULAR ADIPONECTIN; GLUCOSE-HOMEOSTASIS; MITOCHONDRIAL DYSFUNCTION;
D O I
10.2174/157436212800376717
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Insulin resistance (IR) is defined as a decreased response of peripheral tissues to insulin. It is a common cause of cardiovascular and hepatic diseases, and often precedes the onset of hyperglycemia and predicts the development of type 2 diabetes. Free fatty acids (FFA), inflammation and oxidative stress play key roles in the development and/or progression of IR induced by obesity. Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear hormone receptor superfamily; PPAR agonists can improve IR by regulating glucose and lipid metabolisms, and by inhibiting inflammatory and oxidative stress responses. In the article, we will review the pathogenesis of obesity-induced IR, its therapeutic targets: PPAR alpha/gamma, and discuss the signal transduction pathways through which these drugs exert therapeutic effects.
引用
收藏
页码:177 / 184
页数:8
相关论文
empty
未找到相关数据