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Very long-chain-fatty acids enhance adipogenesis through coregulation of Elovl3 and PPARgamma in 3T3-L1 cells


, : Very long-chain-fatty acids enhance adipogenesis through coregulation of Elovl3 and PPARgamma in 3T3-L1 cells.

Here, we show that Elovl3 (elongation of very long-chain fatty acids 3) was involved in the regulation of the progression of adipogenesis through activation of peroxisome proliferator-activated receptor (PPAR) in mouse adipocytic 3T3-L1 cells. The expression of the Elovl3 gene increased during adipogenesis, the expression pattern of which was similar to that of the PPAR gene. Troglitazone, a PPAR agonist, enhanced Elovl3 expression in adipocytes, as it did that of other PPAR target genes. Promoter-reporter analysis demonstrated that three PPAR-responsive elements in the Elovl3 gene promoter had the potential to activate its expression in 3T3-L1 cells. Moreover, a chromatin immunoprecipitation assay revealed that PPAR bound these PPAR-responsive elements of the Elovl3 promoter. When the Elovl3 mRNA level was suppressed by its siRNAs, the level of intracellular triglycerides was significantly decreased, and the expression levels of adipogenic, lipolytic, and lipogenic genes were also repressed. In a mammalian two-hybrid assay, C18:1 and C2:1 very long-chain fatty acids (VLCFAs), which are the products of Elovl3 and activated PPAR function. In addition, these same VLCFAs could prevent the Elovl3 siRNA-mediated suppression of adipogenesis by enhancing the expression of adipogenic, lipolytic, and lipogenic genes in adipocytes. Moreover, this VLCFAs-mediated activation was repressed by a PPAR antagonist. These results indicate that the expression of the Elovl3 gene was activated by PPAR during adipogenesis. Elovl3-produced C18:1 and C2:1 VLCFAs acted as agonists of PPAR in 3T3-L1 cells. Thus, the Elovl3-PPAR cascade is a novel regulatory circuit for the regulation of adipogenesis through improvement of PPAR function in adipocytes.

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