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载脂蛋白 A5 降低与肥胖相关的胰岛素抵抗性高甘油三酯血症有关。

Decreased apolipoprotein A5 is implicated in insulin resistance-related hypertriglyceridemia in obesity.

机构信息

Department of Cardiology, The Second Xiang Ya Hospital, Central South University, No. 139, Renmin Zhonglu, Changsha, Hunan, 410011, China.

出版信息

Atherosclerosis. 2010 Jun;210(2):563-8. doi: 10.1016/j.atherosclerosis.2009.12.004. Epub 2009 Dec 11.

DOI:10.1016/j.atherosclerosis.2009.12.004
PMID:20047745
Abstract

Hypertriglyceridemia is associated insulin resistance in obese people. Recently identified apolipoprotein A5 (apoA5) is involved in triglyceride (TG) metabolism. This study was to investigate the role of apoA5 in insulin resistance-related hypertriglyceridemia in obesity. 682 participants including 340 non-obese individuals and 342 obese individuals were recruited in this study. Plasma apoA5 levels were measured. The insulin resistance in participants was assessed by homeostasis model assessment of insulin resistance (HOMA-IR). An insulin resistant and hypertriglyceridemic rat model was established by high-fructose diet with obese Zucker rats as positive controls. Besides, two insulin resistant models in vitro were induced by insulin and tumor necrosis factor-alpha (TNFalpha) in HepG2 cells. Obese participants had lower plasma apoA5 levels. Plasma apoA5 levels were inversely correlated with TG, body mass index and HOMA-IR in humans. Furthermore, hepatic and plasma apoA5 reduced in fructose-fed rats whereas no significant changes of apoA5 were observed in obese Zucker rats. In addition, treatment of HepG2 cells with insulin and TNFalpha decreased apoA5 expression and increased TG content. Thus, decreased apolipoprotein A5 is implicated in insulin resistance-related hypertriglyceridemia in obesity.

摘要

高甘油三酯血症与肥胖人群的胰岛素抵抗有关。最近发现的载脂蛋白 A5(apoA5)参与了甘油三酯(TG)代谢。本研究旨在探讨 apoA5 在肥胖相关胰岛素抵抗性高甘油三酯血症中的作用。本研究纳入了 682 名参与者,包括 340 名非肥胖者和 342 名肥胖者,测量了他们的血浆 apoA5 水平。采用稳态模型评估胰岛素抵抗(HOMA-IR)评估参与者的胰岛素抵抗情况。以肥胖 Zucker 大鼠为阳性对照,用高果糖饮食建立胰岛素抵抗和高甘油三酯血症大鼠模型。此外,还通过胰岛素和肿瘤坏死因子-α(TNFalpha)在 HepG2 细胞中诱导了两种体外胰岛素抵抗模型。肥胖参与者的血浆 apoA5 水平较低。血浆 apoA5 水平与人类的 TG、体重指数和 HOMA-IR 呈负相关。此外,果糖喂养的大鼠肝组织和血浆 apoA5 减少,而肥胖 Zucker 大鼠中 apoA5 无明显变化。此外,用胰岛素和 TNFalpha 处理 HepG2 细胞可降低 apoA5 的表达并增加 TG 含量。因此,apoA5 的减少与肥胖相关的胰岛素抵抗性高甘油三酯血症有关。

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