Maternal coconut oil intake on lactation programs for endocannabinoid system dysfunction in adult offspring.

Maternal exposure to coconut oil metabolically programs adult offspring for overweight, hyperphagia and hyperleptinemia. We studied the neuroendocrine mechanisms by which coconut oil supplementation during breastfeeding as well as continued exposure of this oil throughout life affect the feeding behavior of the progeny. At birth, pups were divided into two groups: Soybean oil (SO) and Coconut oil (CO). Dams received these oils by gavage (0.5 g/kg body mass/day) during lactation. Half of the CO group continued to receive CO in chow throughout life (CO + C). Adult CO and CO + C groups had overweight; the CO group had hyperphagia, higher visceral adiposity, and hyperleptinemia, while the CO + C group had hypophagia only. The CO group showed higher DAGLα (endocannabinoid synthesis) but no alteration of FAAH (endocannabinoid degradation) or CB1R. Leptin signaling and GLP1R were unchanged in the CO group, which did not explain its phenotype. Hyperphagia in these animals can be due to higher DAGLα, increasing the production of 2-AG, an orexigenic mediator. The CO + C group had higher preference for fat and lower hypothalamic GLP1R content. Continuous exposure to coconut oil prevented an increase in DAGLα. The CO + C group, although hypophagic, showed greater voracity when exposed to a hyperlipidemic diet, maybe due to lower GLP1R, since GLP1 inhibits short-term food intake.