Long-chain-fatty-acid—Co A Ligase - Inhibition By Long Chain Fatty Acyl-CoAs

Inhibition By Long Chain Fatty Acyl-CoAs

A long term and short term regulation controls fatty acid synthesis. Long term fatty acid synthesis regulation is dependent on the rate of acetyl-CoA carboxylase (ACC) synthesis, the rate-limiting enzyme and first enzyme of the fatty acid synthesis, and fatty acid synthase (FAS), the second and major enzyme of the fatty acid synthesis. Cellular fatty acyl-CoA is involved in the short term regulation, but there is not a full understanding of the mechanisms.

Free fatty acids inhibits the de novo fatty acid synthesis and appears to be dependent on the formation of long chain fatty acyl-CoAs. Studies have shown that long chain fatty acyl-CoAs inhibit ACC and FAS via feedback inhibition. Long chain fatty acyl-CoA’s inhibitory effect on the fatty acid synthesis may be a result of its regulation of lipogenic enzymes in a feedback manner through gene transcription suppression.

Long-chain fatty-acid-CoA ligase in cells catalytically synthesizes long chain fatty acyl-CoAs. Long-chain fatty-acid-CoA ligase may be involved in an important role in the suppression of fatty acid synthesis and it has been reported that it played a part in fatty acid synthesis inhibition. It was recently found that vitamin D3 upregulates FACL3, which forms long-chain fatty acid synthesis through the use of myristic acid, eicosapentaenoic acid (EPA), and arachidonic acid as substrates, in expression and activity levels. FACL3 contributes to vitamin D3 growth inhibitory effect in human prostate cancer LNCaP cells. A current study reports that the feedback inhibition of FAS expression by long chain fatty acyl-CoAs causes the downregulation of FAS mRNA by vitamin D3.

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