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注入致动脉粥样硬化脂蛋白颗粒会增加兔子肝脏中的脂肪酶活性。

Infusion of atherogenic lipoprotein particles increases hepatic lipase activity in the rabbit.

作者信息

Ebert D L, Warren R J, Barter P J, Mitchell A

机构信息

Baker Medical Research Institute, Prahran, Victoria, Australia.

出版信息

J Lipid Res. 1993 Jan;34(1):89-94.

PMID:8445346
Abstract

Hepatic lipase plays a key role in the turnover of potentially atherogenic lipoprotein remnants and in determining the relative distribution of high density lipoprotein (HDL) particle size subclasses. Rabbits fed a cholesterol-enriched diet have been found to accumulate potentially atherogenic chylomicron remnants and beta-very low density lipoprotein (beta-VLDL) and show a rapid increase in liver and postheparin plasma hepatic lipase activity. To determine whether the particles that accumulate during cholesterol feeding are a stimulus for this increase in hepatic lipase activity, we infused normal chow-fed rabbits with a chylomicron remnant plus beta-VLDL-enriched plasma fraction isolated from rabbits fed 0.5% cholesterol-supplemented chow. The infusion of this plasma fraction for 4 h increased hepatic lipase activity up to 2.9-fold over control rabbits and resulted in a loss of larger sized HDL particles consistent with the action of hepatic lipase. The increase in activity was significantly correlated with the concentration of infusate phospholipid, unesterified cholesterol, and esterified cholesterol, but not with the infusate triglyceride concentration. The change in the plasma cholesterol concentration of recipient rabbits, which reflects the degree of lipoprotein accumulation in these rabbits, was also significantly correlated with the change in hepatic lipase activity. However, a chylomicron remnant and beta-VLDL-depleted fraction of plasma from cholesterol-fed rabbits did not increase hepatic lipase activity. Furthermore, triglyceride presented as an artificial lipid emulsion (Intralipid) was not able to stimulate hepatic lipase activity, although triglyceride is a substrate for hepatic lipase.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

肝脂酶在潜在致动脉粥样硬化脂蛋白残粒的代谢以及高密度脂蛋白(HDL)颗粒大小亚类的相对分布决定中起关键作用。已发现喂食富含胆固醇饮食的兔子会积累潜在致动脉粥样硬化的乳糜微粒残粒和β-极低密度脂蛋白(β-VLDL),并显示肝脏和肝素后血浆肝脂酶活性迅速增加。为了确定在喂食胆固醇期间积累的颗粒是否是肝脂酶活性增加的刺激因素,我们向正常喂食普通饲料的兔子输注了从喂食0.5%胆固醇补充饲料的兔子中分离出的富含乳糜微粒残粒加β-VLDL的血浆部分。输注该血浆部分4小时后,肝脂酶活性比对照兔子增加了2.9倍,并导致与肝脂酶作用一致的较大尺寸HDL颗粒的减少。活性增加与输注液中磷脂、未酯化胆固醇和酯化胆固醇的浓度显著相关,但与输注液甘油三酯浓度无关。受体兔子血浆胆固醇浓度的变化反映了这些兔子中脂蛋白积累的程度,也与肝脂酶活性的变化显著相关。然而,来自喂食胆固醇兔子的乳糜微粒残粒和β-VLDL耗尽的血浆部分并未增加肝脂酶活性。此外,尽管甘油三酯是肝脂酶的底物,但作为人工脂质乳剂(英脱利匹特)呈现的甘油三酯并不能刺激肝脂酶活性。(摘要截短于250字)

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