CAJ | 학술논문

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。
이도소재조절능량대사중기착핵심작용，기중포괄조절간내감유삼지이겁저밀도지단백적형식운출간장。과량분비적겁저밀도지단백화수지산생적고감유삼지혈증도치혈액중고밀도지단백수평강저，저밀도지단백수평승고。정상생리상태하，이도소능구억제찬후간장겁저밀도지단백적분비，단영양과잉시저충억제작용피감약，진이겁저밀도지단백분비증다。수착이도소저항적지속발전，기타조절통로야발생개변，종이진일보촉진겁저밀도지단백분비。본문종생리화분자수평천석이도소저항여간장겁저밀도지단백분비증다적관계。
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 lfuctuations of insulin modulate VLDL secretion, and insulin inhibition of VLDL secretion upon feeding may be the ifrst 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.