Fatty acid transporter expression in human myocytes

Abstract

Long‐chain fatty acid (LCFA) transporters in skeletal muscle mediate the uptake and subsequent storage and/or oxidation of LCFA in muscle. The purpose of this study was to examine the regulation of LCFA transporter expression in skeletal muscle. We measured the mRNA expression via RT‐PCR of FAT/CD36, FABPPM, and FATP1 in myocytes that were isolated and cultured from lean and morbidly obese subjects. Skeletal muscle FAT/CD36, FABPPM, and FATP1 mRNA expression were significantly upregulated 2‐fold in the morbidly obese myocytes compared to lean. The addition of a PPARγ antagonist at either 2μM or 4μM in the morbidly obese myocytes significantly decreased FAT/CD36 mRNA expression in a dose‐dependent manner by 42% and 66%, respectively. Treatment with fatty acids (100μM) significantly increased mRNA expression of FAT/CD36 (2‐fold), FABPPM (2.5‐fold), and FATP1 (2‐fold) in lean myocytes, whereas LCFA transporter mRNA expression remained upregulated in morbidly obese myocytes. When lean myocytes were incubated in the presence of insulin (10nM), mRNA expression of FAT/CD36 (2‐fold) and FATP1 (1.7‐fold) was significantly increased. We conclude that LCFA transporter expression is upregulated in morbidly obese skeletal muscle and following treatment with fatty acids. Our findings also indicate that FAT/CD36 expression is downregulated in the presence of a PPARγ antagonist.