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首页> 外文期刊>Current opinion in lipidology >Fructose consumption: potential mechanisms for its effects to increase visceral adiposity and induce dyslipidemia and insulin resistance.
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Fructose consumption: potential mechanisms for its effects to increase visceral adiposity and induce dyslipidemia and insulin resistance.

机译:果糖消费:其影响内脏肥胖和诱发血脂异常和胰岛素抵抗的潜在机制。

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摘要

PURPOSE OF REVIEW: Based on interim results from an ongoing study, we have reported that consumption of a high-fructose diet, but not a high-glucose diet, promotes the development of three of the pathological characteristics associated with metabolic syndrome: visceral adiposity, dyslipidemia, and insulin resistance. From these results and a review of the current literature, we present two potential sequences of events by which fructose consumption may contribute to metabolic syndrome. RECENT FINDINGS: The earliest metabolic perturbation resulting from fructose consumption is postprandial hypertriglyceridemia, which may increase visceral adipose deposition. Visceral adiposity contributes to hepatic triglyceride accumulation, novel protein kinase C activation, and hepatic insulin resistance by increasing the portal delivery of free fatty acids to the liver. With insulin resistance, VLDL production is upregulated and this, along with systemic free fatty acids, increase lipid delivery to muscle. It is also possible that fructose initiates hepatic insulin resistance independently of visceral adiposity and free fatty acid delivery. By providing substrate for hepatic lipogenesis, fructose may result in a direct lipid overload that leads to triglyceride accumulation, novel protein kinase C activation, and hepatic insulin resistance. SUMMARY: Our investigation and future studies of the effects of fructose consumption may help to clarify the sequence of events leading to development of metabolic syndrome.
机译:审查目的:根据一项正在进行的研究的中期结果,我们报告说,食用高果糖饮食而非高糖饮食可促进与代谢综合征相关的三种病理特征的发展:内脏脂肪,血脂异常和胰岛素抵抗。从这些结果和对当前文献的回顾中,我们提出了两个潜在事件序列,通过这些事件果糖消耗可能会导致代谢综合征。最新发现:摄入果糖引起的最早的代谢紊乱是餐后高甘油三酯血症,这可能会增加内脏脂肪沉积。内脏脂肪通过增加游离脂肪酸向肝脏的门传递而有助于肝甘油三酸酯的积累,新的蛋白激酶C活化和肝胰岛素抵抗。由于具有胰岛素抵抗性,VLDL的产生被上调,这与全身性游离脂肪酸一起增加了脂质向肌肉的输送。果糖也可以独立于内脏脂肪和游离脂肪酸而引发肝胰岛素抵抗。通过提供肝脏脂肪生成的底物,果糖可能会导致直接的脂质超负荷,从而导致甘油三酸酯积累,新的蛋白激酶C活化和肝胰岛素抵抗。摘要:我们对果糖消费影响的调查和未来研究可能有助于弄清导致代谢综合征发展的事件顺序。

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