High-fat diets are closely implicated in the pathogenesis of chronic conditions, including obesity and hepatic steatosis. Recently, coconut oil, which is rich in medium-chain fatty acids, has attracted significant attention for its potential anti-obesity and anti-inflammatory properties. This study aimed to evaluate the effects of medium-chain fatty acids derived from coconut oil on metabolic disorders, particularly fatty liver, using a mouse model established by a high-fat diet. C57BL/6J mice were assigned to either the lard diet group or the coconut oil diet group and fed for 12 weeks. Glucose tolerance was assessed, and biochemical parameters, liver histology, and gene expression in the liver were analysed. Additionally, the concentrations of medium-chain fatty acids within the liver were determined through gas chromatography-mass spectrometry analysis. Mice fed a coconut oil diet exhibited suppressed weight gain and improved glucose tolerance compared to mice fed a lard diet. Furthermore, the coconut oil diet resulted in reduced hepatic fat accumulation, decreased expression levels of genes implicated in inflammation and lipid metabolism within the liver, and higher concentrations of medium-chain fatty acids in the liver. Coconut oil may contribute to the suppression of hepatic fat accumulation in the liver and the prevention of non-alcoholic fatty liver disease/metabolic dysfunction-associated steatotic liver disease by increasing the levels of medium-chain fatty acids in the liver and suppressing the expression of genes implicated in inflammation and lipid metabolism.

Medium-chain fatty acids (MCFAs) are found at higher levels in milk lipids of many animal species and in the oil fraction of several plants, including coconuts, palm kernels and certain Cuphea species. Medium-chain triglycerides (MCTs) and fatty acids are efficiently absorbed and metabolized and are therefore used for piglet nutrition. They may provide instant energy and also have physiological benefits beyond their energetic value contributing to several findings of improved performance in piglet-feeding trials. MCTs are effectively hydrolyzed by gastric and pancreatic lipases in the newborn and suckling young, allowing rapid provision of energy for both enterocytes and intermediary hepatic metabolism. MCFAs affect the composition of the intestinal microbiota and have inhibitory effects on bacterial concentrations in the digesta, mainly on Salmonella and coliforms. However, most studies have been performed in vitro up to now and in vivo data in pigs are still scarce. Effects on the gut-associated and general immune function have been described in several animal species, but they have been less studied in pigs. The addition of up to 8% of a non-esterified MCFA mixture in feed has been described, but due to the sensory properties this can have a negative impact on feed intake. This may be overcome by using MCTs, allowing dietary inclusion rates up to 15%. Feeding sows with diets containing 15% MCTs resulted in a lower mortality of newborns and better development, particularly of underweight piglets. In conclusion, MCFAs and MCTs offer advantages for the improvement of energy supply and performance of piglets and may stabilize the intestinal microbiota, expanding the spectrum of feed additives supporting piglet health in the post-weaning period.