Regulation of FAT/CD36 mRNA gene expression by long chain fatty acids in the differentiated 3T3-L1 cells
Autor: | Tara J. Loux, Carroll M. Harmon, Min Chen, Yingkui Yang |
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Rok vydání: | 2007 |
Předmět: |
CD36 Antigens
medicine.medical_specialty CD36 Blotting Western Palmitates Cell Line Mice chemistry.chemical_compound Insulin resistance 3T3-L1 Cells Free fatty acid receptor 1 Adipocyte Internal medicine parasitic diseases Adipocytes medicine Animals Insulin RNA Messenger adipocyte protein 2 Cells Cultured chemistry.chemical_classification Analysis of Variance Dose-Response Relationship Drug biology Fatty acid metabolism Reverse Transcriptase Polymerase Chain Reaction business.industry Fatty Acids Isoproterenol Fatty acid General Medicine Blotting Northern medicine.disease Kinetics Endocrinology Gene Expression Regulation chemistry Pediatrics Perinatology and Child Health Free fatty acid receptor biology.protein Surgery business Stearic Acids |
Zdroj: | Pediatric Surgery International. 23:675-683 |
ISSN: | 1437-9813 0179-0358 |
DOI: | 10.1007/s00383-007-1942-6 |
Popis: | 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. |
Databáze: | OpenAIRE |
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