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胆固醇耗竭抑制脂肪酸摄取,而不影响脂肪细胞中CD36或小窝蛋白-1的分布。

Cholesterol depletion inhibits fatty acid uptake without affecting CD36 or caveolin-1 distribution in adipocytes.

作者信息

Covey Scott D, Brunet Rachelle H, Gandhi Shephali G, McFarlane Nicole, Boreham Douglas R, Gerber Gerhard E, Trigatti Bernardo L

机构信息

Department of Biochemistry and Biomedical Sciences, 1200 Main St. W. Hamilton, Ont., Canada L8N 3Z5.

出版信息

Biochem Biophys Res Commun. 2007 Mar 30;355(1):67-71. doi: 10.1016/j.bbrc.2007.01.135. Epub 2007 Feb 2.

Abstract

Caveolin-1 and CD36 are plasma membrane fatty acid binding proteins that participate in adipocyte fatty acid uptake and metabolism. Both are associated with cholesterol-enriched caveolae/lipid rafts in the plasma membrane that are important for long chain fatty acid uptake. Depletion of plasma membrane cholesterol reversibly inhibited oleate uptake by adipocytes without altering the amount or the cell surface distribution of either caveolin-1 or CD36. Cholesterol levels thus regulate fatty acid uptake by adipocytes via a pathway that does not involve altered cell surface localization of caveolin-1 or CD36.

摘要

小窝蛋白-1(Caveolin-1)和CD36是质膜脂肪酸结合蛋白,参与脂肪细胞脂肪酸摄取和代谢。二者都与质膜中富含胆固醇的小窝/脂筏相关,这些小窝/脂筏对长链脂肪酸摄取很重要。质膜胆固醇的耗竭可逆地抑制脂肪细胞对油酸的摄取,而不改变小窝蛋白-1或CD36的数量或细胞表面分布。因此,胆固醇水平通过一条不涉及小窝蛋白-1或CD36细胞表面定位改变的途径调节脂肪细胞的脂肪酸摄取。

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