Regulation of FAT/CD36 mRNA gene expression by long chain fatty acids in the differentiated 3T3-L1 cells

• Published in: Pediatric surgery international Vol. 23; no. 7; pp. 675 - 683
• Main Authors: Yang, Yingkui, Chen, Min, Loux, Tara J, Harmon, Carroll M
• Format: Journal Article
• Language: English
• Published: Germany Springer Nature B.V 01.07.2007
• Subjects: 3T3-L1 Cells; Adipocytes; Adipocytes - metabolism; Analysis of Variance; Animals; Blotting, Northern; Blotting, Western; CD36 Antigens - genetics; Cell Line; Cells, Cultured; Dose-Response Relationship, Drug; Fatty acids; Fatty Acids - metabolism; Gene expression; Gene Expression Regulation - drug effects; Insulin - pharmacology; Insulin resistance; Isoproterenol - pharmacology; Kinetics; Metabolism; Mice; Palmitates - pharmacology; Protein expression; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger - genetics; Stearic Acids - pharmacology
• ISSN: 0179-0358; 1437-9813
• DOI: 10.1007/s00383-007-1942-6

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-gamma, suggesting that FAT/CD36 may have important implications in the pathophysiology of defective fatty acid metabolism.