Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.3.1.28 (chloramphenicol acetyltransferase)
 5,100 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transcriptional regulation of the fatty acid synthase (FAS) gene by insulin/glucose, polyunsaturated fatty acids and leptin was investigated in hepatocytes and adipocytes of Wistar fatty rats and their lean littermates. The sequence spanning nucleotides -57 to -35 of FAS gene, which is responsive to insulin/glucose stimulation [Fukuda, H., Iritani, N. & Noguchi, T. (1997) FEBS Lett. 406, 243-248], was linked to a reporter gene containing a heterologous promoter and transfected into rat hepatocytes or adipocytes. The activity of the reporter, chloramphenicol acetyltransferase, in the presence of glucose alone was similar in the primary cultured cells from the lean and obese rats. In the presence of insulin/glucose, however, chloramphenicol acetyltransferase activity was markedly increased in hepatocytes of lean rats, but was not significantly increased in those of obese rats. The stimulation by insulin/glucose was reduced in arachidonic acid-treated cells of lean rats. Similarly, the stimulation by insulin/glucose was reduced in leptin-treated cells and in cells from lean rats containing an expression vector encoding leptin. However, neither polyunsaturated fatty acids nor leptin-treated cells from obese rats responded to insulin-stimulation. The same effects were observed at endogenous FAS mRNA and enzyme levels. Similar results were seen in adipocytes, although the stimulation and suppression were much smaller than in hepatocytes. The insulin-binding capacities of the receptors of liver and adipose tissue were reduced in the presence of leptin or polyunsaturated fatty acids. Leptin and polyunsaturated fatty acids appeared to suppress the insulin stimulation of FAS transcription by reducing the insulin-binding capacities of receptors. Leptin converged on the insulin/glucose response element of FAS gene and suppressed the transcription.
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PMID:Transcriptional regulation of fatty acid synthase gene by insulin/glucose, polyunsaturated fatty acid and leptin in hepatocytes and adipocytes in normal and genetically obese rats. 1009 88

Transcriptional regulation of ATP citrate-lyase (ACL, one of the lipogenic enzymes) gene by glucose/insulin, polyunsaturated fatty acid (PUFA), and leptin has been investigated in hepatocytes and adipocytes of obese Wistar fatty rats and their lean littermates. The sequence spanning nucleotides -64 to -41 of the ACL gene, which is responsive to glucose/insulin stimulation [Eur. J. Biochem. 247, 497-502, 1997], was linked to a reporter gene and transfected into rat hepatocytes or adipocytes. The chloramphenicol acetyltransferase (CAT) activities in the presence of glucose alone were similar in primary cultured cells from both obese and lean rats. In the presence of glucose/insulin, however, the CAT activities were markedly increased in the hepatocytes of lean rats, but were not significantly increased in those of obese rats. The stimulation by glucose/insulin was reduced in PUFA-treated cells of lean rats. The stimulation was also reduced in leptin-treated cells or ob gene expression vector-containing cells. However, PUFA- or leptin-treated cells from obese rats did not show a significant reduction in insulin stimulation. The same effects were observed at the endogenous mRNA and enzyme levels. Similar results were seen in adipocytes, although the stimulation and suppression levels were much smaller than in hepatocytes. The expression of endogenous insulin receptor in hepatocytes and adipocytes was reduced in the presence of leptin or PUFA. We previously found that insulin-binding capacities are also reduced in the presence of leptin or PUFA and are very low in obese rats in comparison with lean. Moreover, gel mobility shift assays using end-labeled ACL(-64/-41) revealed that nuclear factor(s) including Sp1 bind specifically to the sequence, and DNA-protein complex formation is reduced in the obese rats. Thus, the reductions in the insulin-stimulated ACL transcription may be ascribed in part to reductions in insulin binding to receptors and DNA-protein complex formation.
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PMID:Regulation of ATP citrate-lyase gene expression in hepatocytes and adipocytes in normal and genetically obese rats. 1042 41