Title : Transcriptional activation of hepatic ACSL3 and ACSL5 by oncostatin m reduces hypertriglyceridemia through enhanced beta-oxidation.

Pub. Date : 2007 Oct

PMID : 17761945






3 Functional Relationships(s)
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1 We further show that overexpression of ACSL3 or ACSL5 alone in the absence of OM led to fatty acid partitioning into beta-oxidation. Fatty Acids acyl-CoA synthetase long chain family member 3 Homo sapiens
2 Importantly, we demonstrate that transfection of siRNAs targeted to ACSL3 and ACSL5 abrogated the enhancing effect of OM on fatty acid oxidation in HepG2 cells. Fatty Acids acyl-CoA synthetase long chain family member 3 Homo sapiens
3 CONCLUSIONS: These new findings identify ACSL3 and ACSL5 as OM-regulated genes that function in fatty acid metabolism and suggest a novel cellular mechanism by which OM directly lowers the plasma TG in hyperlipidemic animals through stimulating the transcription of ACSL specific isoforms in the liver. Fatty Acids acyl-CoA synthetase long chain family member 3 Homo sapiens