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Elevated hepatic fatty acid elongase‐5 (Elovl5) attenuates fatty liver in high fat diet induced obese mice

Fatty liver develops in obese individuals because of an imbalance in hepatic triglyceride (TG) synthesis, secretion, hydrolysis and fatty acid oxidation (FAO). High fat diets induce obesity and fatty liver in C57BL/6J mice and lower hepatic C20–22 PUFA and fatty acid elongase‐5 (Elovl5), a key enzyme involved in PUFA synthesis. The role Elovl5 plays in fatty liver was assessed by using a recombinant adenoviral approach to induce hepatic Elovl5 expression in fasted obese mice. Elevated Elovl5 expression increased hepatic C20–22 PUFA, acetyl‐carnitine and several long chain (C14–20) fatty acyl carnitines as well as plasma β‐hydroxybutyrate. This treatment also decreased hepatic TG content, perilipin and ER stress markers, i.e., XBP‐1, ATF6α. Analysis of enzymes involved in TG hydrolysis and FAO revealed that elevated Elovl5 activity increased expression of ATGL, CGI58 and CTP2, but not other TG lipases or enzymes involved in FAO. Elevated Elovl5 also decreased the nuclear abundance of PPARγ2, but not other transcription factors controlling fatty acid and TG synthesis, i.e., SREBP1 & ChREBP, or enzymes involved in VLDL assembly, i.e., MTTP. Thus, increased hepatic C20–22 PUFA content in response to elevated Elovl5 activity attenuated fatty liver by increasing TG hydrolysis and FAO.