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 µL of water for the control group (CV), 100 or 300 µL of CO (CO100 and CO300) and 100 or 300 µL 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-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-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-, 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.

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Studies show that the high fat diet (HFD) exposure during gestation and lactation promotes obesogenic effects in offspring, such as the increase in the intracellular inflammatory signaling. Studies show that activation of α7nAChR by nicotine suppresses the inflammation in adipose tissue and improves the insulin sensitivity in animal model of obesity. The Offspring (28 days) of mothers fed high-fat diet during pregnancy and lactation showed reduced expression of cholinergic receptor α7nAChR in adipose tissue and hypothalamic. This reduction may contribute to an energy imbalance and increased predisposition to obesity.

Maternal obesity can cause deleterious effects to offspring in perinatal period and adult life. Activation of proinflammatory pathways and metabolic disturbs are frequently observed in offspring of obese dams. Cholinergic antiinflammatory pathway participate of control of inflammatory response through a7 subunit nicotinic acetylcoline receptor (a7AChR), JAK2 and STAT3 proteins. Reduced activity of this pathway lead to high level of inflammatory cytokines. The objective was evaluate the effect of maternal consumption of high-fat diet fed during pregnancy and lactation in liver expression of a7AChR, STAT3 proteins and cytokines. We observed high level of a7AchR mRNA but reduced a7AchR protein. Besides nicotine ICV injection incresed liver IL-10 expression in SC-O mice but in HFD-O mice nicotine did not alter the IL-10 expression.