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组织甘油三酯、胰岛素抵抗与胰岛素分泌:对肥胖症高胰岛素血症的影响

Tissue triglycerides, insulin resistance, and insulin production: implications for hyperinsulinemia of obesity.

作者信息

Koyama K, Chen G, Lee Y, Unger R H

机构信息

Center for Diabetes Research, Department of Internal Medicine, University of Texas Southern Medical Center, Dallas 75235, USA.

出版信息

Am J Physiol. 1997 Oct;273(4):E708-13. doi: 10.1152/ajpendo.1997.273.4.E708.

DOI:10.1152/ajpendo.1997.273.4.E708
PMID:9357799
Abstract

Obesity is associated with both insulin resistance and hyperinsulinemia. Initially hyperinsulinemia compensates for the insulin resistance and thereby maintains normal glucose homeostasis. Obesity is also associated with increased tissue triglyceride (TG) content. To determine whether both insulin resistance and hyperinsulinemia might be secondary to increased tissue TG, we studied correlations between TG content of skeletal muscle, liver, and pancreas and plasma insulin, plasma [insulin] x [glucose], and beta-cell function in four rat models with widely varying fat content: obese Zucker diabetic fatty rats, free-feeding lean Wistar rats, hyperleptinemic Wistar rats with profound tissue lipopenia, and rats pair fed to hyperleptinemics. Correlation coefficients >0.9 (P < 0.05) were obtained among TG of skeletal muscle, liver, and pancreas and among plasma insulin, [insulin] x [glucose] product, and beta-cell function as gauged by basal, glucose-stimulated, and arginine-stimulated insulin secretion by the isolated perfused pancreas. Although these correlations cannot prove cause and effect, they are consistent with the hypothesis that the TG content of tissues sets the level of both insulin resistance and insulin production.

摘要

肥胖与胰岛素抵抗及高胰岛素血症均相关。起初,高胰岛素血症可代偿胰岛素抵抗,从而维持正常的葡萄糖稳态。肥胖还与组织甘油三酯(TG)含量增加有关。为了确定胰岛素抵抗和高胰岛素血症是否均继发于组织TG增加,我们在四种脂肪含量差异很大的大鼠模型中研究了骨骼肌、肝脏和胰腺的TG含量与血浆胰岛素、血浆[胰岛素]×[葡萄糖]以及β细胞功能之间的相关性:肥胖的Zucker糖尿病脂肪大鼠、自由进食的瘦Wistar大鼠、具有严重组织脂肪减少的高瘦素血症Wistar大鼠以及与高瘦素血症大鼠配对饲养的大鼠。骨骼肌、肝脏和胰腺的TG之间以及血浆胰岛素、[胰岛素]×[葡萄糖]产物与β细胞功能之间(通过分离灌注胰腺的基础、葡萄糖刺激和精氨酸刺激的胰岛素分泌来衡量)获得了相关系数>0.9(P<0.05)。尽管这些相关性不能证明因果关系,但它们与组织TG含量设定胰岛素抵抗和胰岛素产生水平的假设一致。

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