作者: Andreas Stahl , Qiwei Wu , Angelica M. Ortegon , Bernice Tsang , Holger Doege
DOI: 10.1128/MCB.26.9.3455-3467.2006
关键词: Skeletal muscle 、 Adipocyte 、 Intracellular 、 Insulin 、 adipocyte protein 2 、 Fatty acid 、 Transport protein 、 Endocrinology 、 Biology 、 Fatty Acid Transport Proteins 、 Internal medicine
摘要: Fatty acid transport protein 1 (FATP1), a member of the FATP/Slc27 family, enhances cellular uptake long-chain fatty acids (LCFAs) and is expressed in several insulin-sensitive tissues. In adipocytes skeletal muscle, FATP1 translocates from an intracellular compartment to plasma membrane response insulin. Here we show that insulin-stimulated completely abolished FATP1-null greatly reduced muscle FATP1-knockout animals while basal LCFA by both tissues was unaffected. Moreover, loss function altered regulation postprandial serum LCFA, causing redistribution lipids adipocyte tissue liver, led complete protection diet-induced obesity insulin desensitization. This first vivo evidence can regulate via activation FATPs determine distribution dietary lipids. The strong against desensitization observed suggests as novel antidiabetic target.