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胰岛素抵抗大鼠餐后脂蛋白脂肪酶的调节

Postprandial modulation of lipoprotein lipase in rats with insulin resistance.

作者信息

Boivin A, Montplaisir I, Deshaies Y

机构信息

Department of Physiology, School of Medicine, Laval University, Québec, Canada.

出版信息

Am J Physiol. 1994 Oct;267(4 Pt 1):E620-7. doi: 10.1152/ajpendo.1994.267.4.E620.

Abstract

The purpose of this study was to determine whether the postprandial modulation of lipoprotein lipase (LPL) activity was altered in rats with resistance of glucose metabolism to insulin action induced by a high-fat diet. Relationships between serum insulin and tissue LPL activity were established in rats chronically fed a high-carbohydrate or high-fat diet, and the effects of fasting and intake of meals of habitual and alternate composition were contrasted. The feeding paradigm did not result in the development of obesity. Global resistance of glucose metabolism to insulin brought about by chronic high-fat feeding was confirmed by an intravenous glucose tolerance test. Fasting serum glucose and insulin concentrations were similar in both cohorts, as was LPL activity in retroperitoneal and inguinal white adipose tissues (WAT), the heart, and soleus. A high-carbohydrate meal brought about higher postprandial insulinemia in the cohort chronically fed the high-fat diet. This was associated with larger changes in LPL activity, that is, an increase in inguinal WAT and in brown adipose tissue and a decrease in soleus, red vastus lateralis, and the heart. Thus the established postprandial modulation of LPL, presumably by insulin, was potentiated in the presence of hyperinsulinemia induced by chronic high-fat feeding despite the concomitant impairment of glucose metabolism.

摘要

本研究的目的是确定在因高脂饮食诱导而出现葡萄糖代谢对胰岛素作用抵抗的大鼠中,脂蛋白脂肪酶(LPL)活性的餐后调节是否发生改变。在长期喂食高碳水化合物或高脂饮食的大鼠中建立血清胰岛素与组织LPL活性之间的关系,并对比禁食以及摄入习惯组成和替代组成餐食的影响。喂食模式并未导致肥胖的发生。静脉葡萄糖耐量试验证实了慢性高脂喂养导致的葡萄糖代谢对胰岛素的整体抵抗。两个队列的空腹血糖和胰岛素浓度相似,腹膜后和腹股沟白色脂肪组织(WAT)、心脏和比目鱼肌中的LPL活性也相似。在长期喂食高脂饮食的队列中,高碳水化合物餐导致餐后胰岛素血症更高。这与LPL活性的更大变化相关,即腹股沟WAT和棕色脂肪组织中的LPL活性增加,而比目鱼肌、股外侧肌和心脏中的LPL活性降低。因此,尽管存在慢性高脂喂养诱导的高胰岛素血症以及伴随的葡萄糖代谢受损,但推测由胰岛素介导的已确立的LPL餐后调节在这种情况下得到了增强。

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