Lauric Acid versus Palmitic Acid: Effects on Adipose Tissue Inflammation, Insulin Resistance, and Non-Alcoholic Fatty Liver Disease in Obesity

Simple Summary The aim of this study was to compare the effect of palmitic acid (PA), a long-chain fatty acid, and lauric acid (LA), a medium-chain fatty acid, on obesity-related metabolic disorders. We used a mouse model of diet-induced obesity and fed them a modified high fat diet supplemented with 3% PA or LA for 12 wk. An LA diet led to an increase in visceral fat mass with a reduction in inflammation compared to the PA diet. We also noted that PA significantly increased systemic insulin resistance whereas LA showed only a trend towards an increase compared to lean control mice. The expression of a protein involved in muscle glucose uptake was higher in LA-treated mice compared to the PA-treated group, indicating improved muscle glucose uptake in LA-fed mice. Analysis of liver samples showed that hepatic steatosis was higher in both PA and LA-fed mice compared to lean controls. Markers of liver inflammation were not altered significantly in mice receiving PA or LA. Our data suggest that compared to PA, LA exerts less adverse effects on metabolic disorders and this could be due to the differential effects of these fatty acids in fat and muscle. Coconut oil, rich in medium-chain saturated fatty acids (MCSFA), in particular, lauric acid (LA), is known to exert beneficial metabolic effects. Although LA is the most abundant saturated fatty acid in coconut oil, the specific role of LA in altering obesity-related metabolic disorders remains unknown. Here, we examined the effects of supplementing a high fat (HF) diet with purified LA on obesity-associated metabolic derangements in comparison with palmitic acid (PA), a long-chain saturated fatty acid. Male C57BL/6 mice were fed a control chow diet (CD) or an HF diet supplemented with 3% LA (HF + LA) or PA (HF + PA) for 12 wk. Markers of adipose tissue (AT) inflammation, systemic insulin resistance (IR), and hepatic steatosis, were assessed. The body weight and total fat mass were significantly higher in both HF + LA and HF + PA diet-fed groups compared to CD controls. However, the visceral adipose tissue (VAT) mass was significantly higher (p < 0.001) in HF + LA-fed mice compared to both CD as well as HF + PA-fed mice. Interestingly, markers of AT inflammation were promoted to a lesser extent in HF + LA-fed mice compared to HF + PA-fed mice. Thus, immunohistochemical analysis of VAT showed an increase in MCP-1 and IL-6 staining in HF + PA-fed mice but not in HF + LA-fed mice compared to CD controls. Further, the mRNA levels of macrophage and inflammatory markers were significantly higher in HF + PA-fed mice (p < 0.001) whereas these markers were increased to a lesser extent in HF + LA-fed group. Of note, the insulin tolerance test revealed that IR was significantly increased only in HF + PA-fed mice but not in HF + LA-fed group compared to CD controls. While liver triglycerides were increased significantly in both HF + PA and HF + LA-fed mice, liver weight and plasma markers of liver injury such as alanine aminotransferase and aspartate aminotransferase were increased significantly only in HF + PA-fed mice but not in HF + LA-fed mice. Taken together, our data suggest that although both LA and PA increased AT inflammation, systemic IR, and liver injury, the extent of metabolic derangements caused by LA was less compared to PA in the setting of high fat feeding.