Palmitoleate Supplementation Dissociates Liver Inflammatory Response from Hepatic Steatosis in Mice

Supplementation of monounsaturated fatty acids generates beneficial effects. We investigated the effects of palmitoleate supplementation on liver inflammatory and metabolic responses. At 5 – 6 weeks of age, male wild‐type C57BL6/J mice were fed a low‐fat diet (LFD) for 12 weeks and supplemented with palmitoleate (600mg/kg/d), oleate (600mg/kg/d), or bovine serum albumin (BSA) via oral gavages for the last 4 weeks. Compared with controls, palmitoleate supplementation increased circulating levels of palmitoleate and improved systemic insulin sensitivity. Locally, palmitoleate supplementation increased hepatic fat deposition and the expression of sterol regulatory element‐binding protein 1c and fatty acid synthase. However, palmitoleate supplementation reduced the numbers of macrophages/Kupffer cells in livers of the treated mice. Consistently, supplementation of palmitoleate, but not oleate or BSA, decreased the phosphorylation of nuclear factor kappa B and the expression of tumor necrosis factor alpha and interleukin‐6 in livers. Together, these findings demonstrate a novel role for palmitoleate supplementation in dissociating liver inflammatory response from hepatic steatosis. When used with anti‐steatosis agents, palmitoleate supplementation may be a viable approach to preventing liver inflammation. Grant Funding Source : ADA