食物摄入后残余脂蛋白中甘油三酯显著增加及其与血浆脂蛋白脂肪酶的关系

K. Nakajima, Y. Tokita, A. Tanaka
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摘要

本文介绍了餐后极低密度脂蛋白(VLDL)残余物(残体脂蛋白;RLP作为甘油三酯(TG)增加的主要成分,在脂肪负荷后显著增加,并参与肥胖和胰岛素抵抗。长期以来,人们一直认为餐后RLP(主要是乳糜微粒(chylommicron, CM)残余物)的增加是由于胰岛素抵抗等引起的脂蛋白脂肪酶(LPL)活性紊乱所致。然而,基于该报告,我们最近提出,当持续暴露于[1]时,由食物摄入产生的餐后VLDL残留物(如过量的脂肪和果糖)升高会导致肥胖和胰岛素抵抗。VLDL残体,而不是CM残体,是本文的关键词,VLDL残体在食物摄入和代谢之间起着决定性的“桥梁”作用。在这里,我们解释了VLDL残留物在食物摄入习惯和体内代谢之间的桥梁作用。从以下6个方面解释了高脂肪膳食摄入与餐后血浆TG和RLP升高之间的关系。(1)为什么TG和RLP在进食后增加?(2)哪些脂蛋白在进食后增加最多?(3)餐后增加的TG由RLP-TG组成的百分比是多少?(4) LPL如何代谢增加的TG ?(5)餐后RLP升高是肥胖和胰岛素抵抗的结果还是肥胖和胰岛素抵抗的原因?(6)为什么餐后TG是心血管疾病的风险因素?
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Triglyceride is Significantly Increased in Remnant Lipoproteins After Food Intake and its Association with Lipoprotein Lipase in the Plasma
This article introduces the characteristics of postprandial Very Low Density Lipoprotein (VLDL) remnants (remnant lipoproteins; RLP) in plasma which significantly increased after fat load as a major component of increased Triglycerides (TG) and involved in obesity and insulin resistance. It has been long believed that postprandial RLP, mainly Chylomicron (CM) remnants, increases as the result of disturbed lipoprotein lipase (LPL) activity caused by insulin resistance, etc. However, based on this report, we recently proposed that elevated postprandial VLDL remnants produced by food intake, such as excessive fat and fructose, cause obesity and insulin resistance when exposed continuously [1]. VLDL remnants, but not CM remnants, is the key word of this article and VLDL remnants play a definitive role as a “bridge” between food intake and its metabolism. Here, we have explained the bridging role of VLDL remnants between the habit of food intake and its metabolism in body. Following 6 aspects between fat-rich meal intake and the increase of plasma postprandial TG and RLP are explained. (1) Why TG and RLP increase after food intake? (2) Which lipoproteins increase most after food intake? (3) What percentage of increased TG after food is comprised of RLP-TG? (4) How the increased TG is metabolized by LPL? (5) The increase of postprandial RLP is the result of obesity and insulin resistance or cause of obesity and insulin resistance? (6)Why postprandial TG is a risk of cardiovascular diseases?
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