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肥胖 Zucker 大鼠心肌细胞中脂肪酸转运蛋白(FAT)/CD36 介导的长链脂肪酸摄取增加。

Increased FAT (fatty acid translocase)/CD36-mediated long-chain fatty acid uptake in cardiac myocytes from obese Zucker rats.

作者信息

Coort S L M, Luiken J J F P, van der Vusse G J, Bonen A, Glatz J F C

机构信息

Department of Molecular Genetics, Cardiovascular Research Institute Maastricht, Maastricht University, P.O. Box 616, NL-6200 MD Maastricht, The Netherlands.

出版信息

Biochem Soc Trans. 2004 Feb;32(Pt 1):83-5. doi: 10.1042/bst0320083.

Abstract

Disturbed cardiac lipid homoeostasis in obesity is regarded as a key player in the development of cardiovascular diseases. In this study, we show that FAT (fatty acid translocase)/CD36-mediated LCFA (long-chain fatty acid) uptake in cardiac myocytes from young adult obese Zucker rats is markedly increased, but insensitive to insulin. Basal and insulin-induced glucose uptake rates in these myocytes are not changed, suggesting that during the development from obesity to hyperglycaemic Type II diabetes, alterations in cardiac LCFA uptake precede alterations in cardiac glucose uptake.

摘要

肥胖状态下心脏脂质稳态紊乱被认为是心血管疾病发生发展的关键因素。在本研究中,我们发现,成年早期肥胖Zucker大鼠心肌细胞中,脂肪酸转运蛋白(FAT)/CD36介导的长链脂肪酸(LCFA)摄取显著增加,但对胰岛素不敏感。这些心肌细胞的基础葡萄糖摄取率和胰岛素诱导的葡萄糖摄取率未发生变化,这表明在从肥胖发展到高血糖II型糖尿病的过程中,心脏LCFA摄取的改变先于心脏葡萄糖摄取的改变。

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