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Hepatic long‐chain acyl‐CoA synthetase 5 (ACSL5) partitions fatty acids between anabolic and catabolic pathways

Long‐chain acyl‐CoA synthetases (ACSL) and fatty acid transport proteins (FATP) catalyze the initial step of fatty acid metabolism. Of numerous ACSL and FATP isoforms, ACSL5 is expressed predominantly in tissues with high rates of TAG synthesis suggesting it may have an anabolic role in lipid metabolism. To characterize the role of ACSL5 in hepatic energy metabolism, we knocked down ACSL5 by using siRNA in rat primary hepatocytes. Compared to cells transfected with control siRNA, knockdown of ACSL5 significantly decreased fatty acid or glucose induced lipid droplet formation observed by Oil‐red O staining. These findings were further extended with metabolic labeling studies showing that ACSL5 knockdown resulted in decreased [1‐14C] oleic acid or acetic acid incorporation into intracellular glycerolipids (30–50%) without altering fatty acid uptake. ACSL5 knockdown increased acid soluble metabolites (ASM), a measure of fatty acid β‐oxidation, without changing PPAR‐α activity and target gene expression indicating that the effect was not mediated by transcriptional regulation. These changes in fatty acid metabolism were similar during pulse and chase periods, which indicate that ACSL5 may not affect intracellular lipid turnover. These results suggest that ACSL5 has a unique role in channeling both exogenous and endogenous fatty acid towards glycerolipid synthesis rather than catabolic pathways.