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膳食果糖或葡萄糖对Wistar肥胖大鼠(非胰岛素依赖型糖尿病动物模型)肝脏中甘油三酯生成及脂肪生成酶活性的影响。

Effects of dietary fructose or glucose on triglyceride production and lipogenic enzyme activities in the liver of Wistar fatty rats, an animal model of NIDDM.

作者信息

Kazumi T, Odaka H, Hozumi T, Ishida Y, Amano N, Yoshino G

机构信息

Department of Medicine, Hyogo Rehabilitation Center Hospital, Kobe, Japan.

出版信息

Endocr J. 1997 Apr;44(2):239-45. doi: 10.1507/endocrj.44.239.

Abstract

Effects of dietary carbohydrates on triglyceride production and hepatic lipogenic enzyme activities were examined in Wistar fatty rats, an animal model of noninsulin dependent diabetes mellitus, fed fructose or glucose and were compared with those of Wistar lean rats. Carbohydrates were supplied in 10% drinking solutions for 21 days. As compared with lean rats, Wistar fatty rats were characterized by hyperglycemia, hyperinsulinemia and hypertriglyceridemia, the last of which was associated with an increased hepatic activity of fatty acid synthetase and an increased rate of triglyceride secretion from the liver to the circulation. Feeding fructose to genetically obese diabetic rats produced a threefold increase in the hepatic activity of fatty acid synthetase, a twofold increase in NADPH-generating enzymes (malic enzyme and glucose-6-phosphate dehydrogenase) and a 56% increase in the rate of triglyceride secretion, with a resultant 86% increase in plasma triglyceride concentrations. Feeding glucose produced a similar increase in the activity of NADPH-generating enzymes and triglyceride production in the fatty liver but it differed in producing no change in plasma triglyceride concentrations or hepatic fatty acid synthetase activity. Neither dietary fructose nor glucose changed glycemia or insulinemia. These results show that in genetically obese, diabetic rats feeding fructose and glucose is associated with an increase in hepatic lipogenic enzyme activities and triglyceride production, and suggest that fructose stimulates triglyceride production but impairs triglyceride removal, whereas glucose stimulates both of them.

摘要

在非胰岛素依赖型糖尿病动物模型Wistar肥胖大鼠中,研究了膳食碳水化合物对甘油三酯生成及肝脏脂肪生成酶活性的影响。将Wistar肥胖大鼠喂食果糖或葡萄糖,并与Wistar瘦大鼠进行比较。碳水化合物以10%的饮水溶液形式提供21天。与瘦大鼠相比,Wistar肥胖大鼠的特征为高血糖、高胰岛素血症和高甘油三酯血症,其中后者与肝脏脂肪酸合成酶活性增加以及肝脏向循环系统分泌甘油三酯的速率增加有关。给遗传性肥胖糖尿病大鼠喂食果糖后,肝脏脂肪酸合成酶活性增加了两倍,产生NADPH的酶(苹果酸酶和葡萄糖-6-磷酸脱氢酶)增加了一倍,甘油三酯分泌速率增加了56%,血浆甘油三酯浓度因此增加了86%。喂食葡萄糖使脂肪肝中产生NADPH的酶活性和甘油三酯生成有类似增加,但不同的是,血浆甘油三酯浓度或肝脏脂肪酸合成酶活性没有变化。膳食果糖和葡萄糖均未改变血糖或胰岛素水平。这些结果表明,在遗传性肥胖糖尿病大鼠中,喂食果糖和葡萄糖与肝脏脂肪生成酶活性及甘油三酯生成增加有关,提示果糖刺激甘油三酯生成但损害甘油三酯清除,而葡萄糖则同时刺激二者。

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