摘要
胰岛素在调节能量代谢中起着核心作用,其中包括调节肝内甘油三酯以极低密度脂蛋白的形式运出肝脏。过量分泌的极低密度脂蛋白和随之产生的高甘油三酯血症导致血液中高密度脂蛋白水平降低,低密度脂蛋白水平升高。正常生理状态下,胰岛素能够抑制餐后肝脏极低密度脂蛋白的分泌,但营养过剩时这种抑制作用被减弱,进而极低密度脂蛋白分泌增多。随着胰岛素抵抗的持续发展,其他调节通路也发生改变,从而进一步促进极低密度脂蛋白分泌。本文从生理和分子水平阐释胰岛素抵抗与肝脏极低密度脂蛋白分泌增多的关系。
Insulin plays a central role in regulating energy metabolism, including hepatic transport of very low-density lipoprotein（VLDL）–associated triglyceride. Hepatic hypersecretion of VLDL and consequent hypertriglyceridemia lead to lower circulation of high-density lipoprotein levels and generation of small dense low-density lipoproteins. Physiological fluctuations of insulin modulate VLDL secretion, and insulin inhibition of VLDL secretion upon feeding may be the first pathway to become resistant in obesity that leads to VLDL hypersecretion. As insulin resistance（IR） progresses, a number of pathways are altered that further augment VLDL hypersecretion. Here, we link IR with increased VLDL secretion at both the physiologic and molecular levels.
出处
《上海医药》
CAS
2014年第13期50-52,共3页
Shanghai Medical & Pharmaceutical Journal
关键词
胰岛素
胰岛素抵抗
极低密度脂蛋白
高甘油三脂血症
分泌
insulin
insulin resistance
very low density lipoprotein
hypertriglyceridaemia
secretion
