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首页> 外文期刊>Endocrine journal >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
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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

机译:饮食中的果糖或葡萄糖对NIDDM动物模型Wistar肥胖大鼠肝中甘油三酸酯生成和脂肪酶活性的影响

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References(27) Cited-By(10) 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.
机译:参考文献(27)被引用(10)在Wistar脂肪大鼠,非胰岛素依赖型糖尿病动物,喂食果糖或葡萄糖的动物模型中,研究了饮食碳水化合物对甘油三酸酯生成和肝脂肪酶活性的影响,并与Wistar lean进行了比较大鼠。碳水化合物以10%的饮用溶液形式供应21天。与瘦大鼠相比,Wistar脂肪大鼠的特点是高血糖,高胰岛素血症和高甘油三酸酯血症,最后一次与脂肪酸合成酶的肝活性增加和从肝脏到循环的甘油三酸酯分泌率增加有关。向遗传性肥胖的糖尿病大鼠喂食果糖可使脂肪酸合成酶的肝脏活性增加三倍,使产生NADPH的酶(苹果酸酶和葡萄糖-6-磷酸脱氢酶)增加三倍,甘油三酸酯分泌速率增加56%。 ,导致血浆甘油三酸酯浓度增加86%。进食葡萄糖会在脂肪肝中产生类似NADPH的酶,增加甘油三酯的生成,但在血浆甘油三酸酯浓度或肝脂肪酸合成酶的活性方面没有变化。饮食中的果糖和葡萄糖都不会改变血糖或胰岛素血症。这些结果表明,在遗传性肥胖的糖尿病大鼠中,喂食果糖和葡萄糖的糖尿病大鼠肝脏脂肪酶活性和甘油三酸酯的产生增加,这表明果糖刺激了甘油三酸酯的产生,但损害了甘油三酸酯的去除,而葡萄糖刺激了两者。

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