CD36
过氧化物酶体
脂肪酸
脂肪酸代谢
过氧化物酶体增殖物激活受体
脂肪细胞蛋白2
生物
生物化学
脂肪组织
β氧化
脂质代谢
胰岛素抵抗
游离脂肪酸受体1
内分泌学
内科学
受体
胰岛素
医学
兴奋剂
作者
Jan F. C. Glatz,Joost J.F.P. Luiken
出处
期刊:Biochimie
[Elsevier]
日期:2017-05-01
卷期号:136: 21-26
被引量:157
标识
DOI:10.1016/j.biochi.2016.12.007
摘要
The molecular mechanisms underlying the cellular uptake of long-chain fatty acids and the regulation of this process have been elucidated in appreciable detail in the last decades. Two main players in this field, each discovered in the early 1990s, are (i) a membrane-associated protein first identified in adipose ('fat') tissue and referred to as putative fatty acid translocase (FAT)/CD36 (now officially designated as SR-B2) which facilitates the transport of fatty acids across the plasma membrane, and (ii) the family of transcription factors designated peroxisome proliferator-activated receptors (PPARα, PPARγ, and PPARβ/δ) for which fatty acids and fatty acid metabolites are the preferred ligand. CD36/SR-B2 is the predominant membrane protein involved in fatty acid uptake into intestinal enterocytes, adipocytes and cardiac and skeletal myocytes. The rate of cellular fatty acid uptake is regulated by the subcellular vesicular recycling of CD36/SR-B2 from endosomes to the plasma membrane. Fatty acid-induced activation of PPARs results in the upregulation of the expression of genes encoding various proteins and enzymes involved in cellular fatty acid utilization. Both CD36/SR-B2 and the PPARs have been implicated in the derangements in fatty acid and lipid metabolism occurring with the development of pathophysiological conditions, such as high fat diet-induced insulin resistance and diabetic cardiomyopathy, and have been suggested as targets for metabolic intervention. In this brief review we discuss the discovery and current understanding of both CD36/SR-B2 and the PPARs in metabolic homeostasis.
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