摘要
近年来,在原发性高血压病人和部分高血压动物模型中发现胰岛素抵抗的存在。在原发性高血压的发生发展中,肾素-血管紧张素系统中的血管紧张素II可促进胰岛素抵抗,涉及到PI3K通路,作用于胰岛素下游通路的Akt和Glut4,进而影响了葡萄糖的利用,导致了胰岛素抵抗。本文从基础及临床两方面,阐明ARB与ACEI改善高血压胰岛素抵抗的可能机制,为临床开展ARB与ACEI改善胰岛素抵抗提供依据。
Recently,Insulin resistance is found in essential hypertension patients and parts of hypertensive animal models.During the course of primary hypertension development,angiotensin II promotes insulin resistance,involving the approach of PI3K which plays an important role in the Akt and Glut4 of insulin downstream pathway,influences the application of glucose and results in insulin resistance.This paper demonstrate the possible mechanism of ARB and ACEI of improving insulin resistance of hypertension patients from basical and clinical aspects,providing evidence for the improvement of insulin resistance by ARB and ACEI in clinical works.
出处
《内蒙古医学院学报》
2011年第1期80-84,共5页
Acta Academiae Medicinae Neimongol
基金
春晖计划(Z2007-1-01008)
关键词
原发性高血压
胰岛素抵抗
RAS系统
PI3K
essential hypertension
insulin resistance
RAS system
Phosphoinositide 3-Kinase
