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Aim:  We aimed to investigate whether maternal malnutrition during gestation/lactation induces long-lasting changes on inflammation, lipid metabolism and endocannabinoid signaling in the adult offspring hypothalamus and the role of hypothalamic astrocytes in these changes. Methods:  We analyzed the effects of a free-choice hypercaloric palatable diet (P) during (pre)gestation, lactation and/or post-weaning on inflammation, lipid metabolism and endogenous cannabinoid signaling in the adult offspring hypothalamus. We also evaluated the response of primary hypothalamic astrocytes to palmitic acid and anandamide. Results:  Postnatal exposure to a P diet induced factors involved in hypothalamic inflammation ( Tnfa  and  Il6 ) and gliosis ( Gfap, vimentin  and  Iba1 ) in adult offspring, being more significant in females. In contrast, maternal P diet reduced factors involved in astrogliosis ( vimentin ), fatty acid oxidation ( Cpt1a ) and monounsaturated fatty acid synthesis ( Scd1 ). These changes were accompanied by an increase in the expression of the genes for the cannabinoid receptor ( Cnr1 ) and  Nape-pld,  an enzyme involved in endocannabinoid synthesis, in females and a decrease in the endocannabinoid degradation enzyme  Faah  in males. These changes suggest that the maternal P diet results in sex-specific alterations in hypothalamic endocannabinoid signaling and lipid metabolism. This hypothesis was tested in hypothalamic astrocyte cultures, where palmitic acid (PA) and the polyunsaturated fatty acid N-arachidonoylethanolamine (anandamide or AEA) were found to induce similar changes in the endocannabinoid system (ECS) and lipid metabolism. Conclusion:  These results stress the importance of both maternal diet and sex in long term metabolic programming and suggest a possible role of hypothalamic astrocytes in this process.

nutritional neuroscience

Maternal hypercaloric diet affects factors involved in lipid metabolism and the endogenous cannabinoid systems in the hypothalamus of adult offspring: sex-specific response of astrocytes to palmitic acid and anandamide