Regulation of FAT/CD36 mRNA gene expression by long chain fatty acids in the differentiated 3T3-L1 cells |
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Authors: | Yingkui Yang Min Chen Tara J Loux Carroll M Harmon |
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Institution: | (1) Department of Surgery, University of Alabama at Birmingham, Birmingham, AL 35205, USA;(2) Department of Pediatric Surgery, University of Alabama at Birmingham, 300 ACC, 1600 7th Avenue South, Birmingham, AL 35205, USA |
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Abstract: | Defects in fatty acid translocase (FAT/CD36) have been identified as a major factor in insulin resistance and defective fatty
acid and glucose metabolism. Therefore, understanding of the regulation of FAT/CD36 expression and function is important for
a potential therapeutic target for type II diabetes. We differentiated 3T3-L1 preadipocytes into matured adipocytes and examined
the roles of insulin and long chain fatty acids on FAT/CD36 expression and function. Our results indicate that FAT/CD36 mRNA
expression was not detected at preadipocyte but was significantly increased at matured adipocyte. In fully differentiated
3T3-L1 adipocytes, insulin significantly increased FAT/CD36 mRNA and protein expression in a dose dependent manner. The free
fatty acid stearic acid reduced FAT/CD36 mRNA expression while the non-metabolizable free fatty acid alpha-bromopalmitate
(2-BP) significantly increased FAT/CD36 mRNA and protein expression. Isoproterenol, in contrast, dose-dependently reduced
FAT/CD36 mRNA expression and increased free fatty acid release. Mechanism analysis indicated that the effect of insulin and
2-BP on the FAT/CD36 mRNA gene expression may be mediated through activation of PPAR-γ, suggesting that FAT/CD36 may have
important implications in the pathophysiology of defective fatty acid metabolism. |
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