Low-Dose Coconut Oil Supplementation Induces Hypothalamic Inflammation, Behavioral Dysfunction, and Metabolic Damage in Healthy Mice

Scope Coconut oil (CO) diets remain controversial due to the possible association with metabolic disorder and obesity. This study investigates the metabolic effects of a low amount of CO supplementation. Methods and Results Swiss male mice are assigned to be supplemented orally during 8 weeks with 300 mu L of water for the control group (CV), 100 or 300 mu L of CO (CO100 and CO300) and 100 or 300 mu L of soybean oil (SO; SO100 and SO300). CO led to anxious behavior, increase in body weight gain, and adiposity. In the hypothalamus, CO and SO increase cytokines expression and pJNK, pNFKB, and TLR4 levels. Nevertheless, the adipose tissue presented increases macrophage infiltration, TNF-alpha and IL-6 after CO and SO consumption. IL-1B and CCL2 expression, pJNK and pNFKB levels increase only in CO300. In the hepatic tissue, CO increases TNF-alpha and chemokines expression. Neuronal cell line (mHypoA-2/29) exposed to serum from CO and SO mice shows increased NFKB migration to the nucleus, TNF-alpha, and NFKBia expression, but are prevented by inhibitor of TLR4 (TAK-242). Conclusions These results show that a low-dose CO changes the behavioral pattern, induces inflammatory pathway activation, TLR4 expression in healthy mice, and stimulates the pro-inflammatory response through a TLR4-mediated mechanism.

Automated summary

The study found that supplementation with a low dose of coconut oil can lead to anxious behavior, weight gain, and adiposity, as well as induce inflammatory responses in the brain and adipose tissue. Furthermore, at a low dose, coconut oil can also activate pro-inflammatory pathways through a TLR4-mediated mechanism.