4.4 Article Proceedings Paper

Regulation of liver carnitine palmitoyltransferase I gene expression by hormones and fatty acids

期刊

BIOCHEMICAL SOCIETY TRANSACTIONS
卷 29, 期 -, 页码 310-316

出版社

PORTLAND PRESS
DOI: 10.1042/BST0290310

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long-chain fatty acids; pancreatic and thyroid hormones; PPAR; transcription

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This brief review focuses on the transcriptional regulation of liver carnitine palmitoyltransferase I (L-CPT I) by pancreatic and thyroid hormones and by long-chain fatty acids (LCFA). Both glucagon and 3,3 ' ,5-tri-iodothyronine (T-3) enhanced the transcription of the gene encoding L-CPT I, whereas insulin had the opposite effect. Interestingly, the transcriptional effect of T-3 required, in addition to the thyroid-responsive element, the co-operation of a sequence located in the first intron of L-CPT I gene. Non-esterified fatty acids rather than acyl-CoA ester or intramitochondrial metabolite were responsible for the transcriptional effect on the gene encoding L-CPT I. It was shown that LCFA and peroxisome proliferators stimulated L-CPT I gene transcription by distinct mechanisms, Peroxisome proliferator stimulated L-CPT I gene transcription through a peroxisome-proliferator-responsive element (PPRE) located at -2846bp, whereas LCFA induced L-CPT I gene transcription through a peroxisome-proliferator-activated receptor a (PPAR alpha)-independent mechanism owing to a sequence located in the first intron of the gene.

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