摘要
胰岛素抵抗(insulin resistance,IR)是指外周组织对胰岛素的反应敏感性降低,是肝脏疾病和心血管病发生的共同基础,常常是高脂血症和2型糖尿病发病的前奏.过氧化物酶体增殖物激活受体(peroxisome proliferator-activated receptors,PPARs)属于核受体超家族的成员.PPARs激动剂可通过多种途径改善胰岛素敏感性,例如调节糖脂代谢、抗炎作用以及间接地改善氧化应激状态.这篇综述主要是回顾IR的病理机制及其治疗靶点:PPARα,δ和γ,并阐明针对此类靶点的胰岛素增敏药物的信号转导通路.
Insulin resistance (IR) is manifested as the decreased response of the peripheral tissues to insulin. IR is an important pathophysiological mechanism in the development of hepatic diseases and cardiovascular disease. IR is also a preclinical indication of hyperlipemia and type 2 diabetes, where a variety of different molecular mechanisms are involved. The peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors belong to the nuclear receptor superfamily. PPARs agonists alleviate IR by regulating glucose and lipid metabolisms, including inhibition of inflammation and oxidative stress responses. In this review we discuss the pathogenesis of obesityinduced IR, focusing on its potential therapeutic targets: PPARα, γ and δ, as well as the related drugs with the signal transduction pathways to mediate their functions.
出处
《中国生物化学与分子生物学报》
CAS
CSCD
北大核心
2014年第6期543-548,共6页
Chinese Journal of Biochemistry and Molecular Biology
基金
无锡市科技发展指导性计划(No.SCZ00N1133)资助~~
关键词
胰岛素抵抗
糖尿病
治疗靶点
过氧化物酶体增殖物激活受体
insulin resistance
diabetes
therapeutic targets
peroxisome proliferator-activated receptors (PPARs)