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糖尿病和代谢综合征中肠道脂蛋白代谢的改变。

Alterations of intestinal lipoprotein metabolism in diabetes mellitus and metabolic syndrome.

作者信息

Arca Marcello

机构信息

Department of Internal Medicine and Medical Specialties, UOS Atherosclerosis Center, La Sapienza University of Rome, Rome, Italy.

出版信息

Atheroscler Suppl. 2015 Feb;17:12-6. doi: 10.1016/S1567-5688(15)50004-4.

Abstract

Diabetes and metabolic syndrome are associated with abnormal postprandial lipoprotein metabolism, with a significant delay in the clearance of many lipid parameters, including triglycerides and chylomicrons. Abnormal concentrations of plasma lipids can result from changes in the production, conversion, or catabolism of lipoprotein particles. Whereas the liver is involved in controlling serum lipid levels through synthesis of liver derived triglyceride-rich lipoproteins and low-density lipoprotein metabolism, the intestine also has a major role in lipoprotein production. Postprandial lipemia results from increases in apoB-48 availability, lipogenesis, and the synthesis and absorption of cholesterol in the enterocytes. Increased intestinal lipoprotein production prolongs postprandial lipemia in patients with diabetes and MetS, and may contribute directly to atherogenesis in these patients.

摘要

糖尿病和代谢综合征与餐后脂蛋白代谢异常有关,许多脂质参数(包括甘油三酯和乳糜微粒)的清除会显著延迟。血浆脂质浓度异常可能源于脂蛋白颗粒的产生、转化或分解代谢的变化。肝脏通过合成富含甘油三酯的肝脏源性脂蛋白和低密度脂蛋白代谢来控制血清脂质水平,而肠道在脂蛋白产生中也起主要作用。餐后血脂异常是由于载脂蛋白B-48可用性增加、脂肪生成以及肠细胞中胆固醇的合成和吸收增加所致。肠道脂蛋白产生增加会延长糖尿病和代谢综合征患者的餐后血脂异常,并且可能直接导致这些患者的动脉粥样硬化。

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