动物模型中的底物竞争和胰岛素作用。

R Vettor, A M Lombardi, R Fabris, R Serra, C Pagano, C Macor, G Federspil
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引用次数: 17

摘要

基础血浆游离脂肪酸和乳酸浓度升高常出现在肥胖中,并可能深刻影响胰岛素的作用。葡萄糖转运或磷酸化的抑制被认为参与了这一现象,但其基础的分子机制尚不清楚。在我们的实验室中,我们观察到长期输注脂内加肝素可以显著降低大鼠的胰岛素依赖型葡萄糖摄取,以及肌肉组织中GLUT4基因的表达。另一方面,已证明血浆乳酸浓度的增加可增加胰岛素分泌和肝脏胰岛素清除率。此外,我们观察到大鼠慢性高乳酸血症能够减少肌肉中的葡萄糖摄取,同时减少相同组织中的GLUT4 mRNA和蛋白。在肥胖中,内脏脂肪产生的乳酸和游离脂肪酸过量可能在降低胰岛素敏感性方面发挥协同作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Substrate competition and insulin action in animal models.

Increased basal plasma FFA and lactate concentrations are often present in obesity and may deeply affect insulin action. The inhibition of glucose transport or phosphorylation is thought to be involved in this phenomenon, but the molecular mechanisms on the basis are still unknown. In our laboratory we observed that a chronic infusion of Intralipid plus heparin in rats significantly decreased the insulin dependent-glucose uptake, as well as GLUT4 gene expression in muscular tissue. On the other hand it has been shown that an enhanced plasma lactate concentration may increase insulin secretion and hepatic insulin clearance. Moreover we observed that chronic hyperlactatemia in rats is able to decrease glucose uptake in muscles, while reducing GLUT4 mRNA and protein in the same tissues. In obesity, lactate and FFA overproduction from visceral fat may therefore play a synergic role in reducing insulin sensitivity.

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