Maternal high-fat diet programs the endocannabinoid system in the small intestine of rat offspring associated with altered endocannabinoid-like compounds in feces and early obesity at weaning

The small intestine regulates the energy balance by several signals, including modulation of the endocannabinoid system (ECS). Endocannabinoids are lipids that activate the type 1 (CB1) and the type 2 (CB2) cannabinoid receptors and they are degraded by specific enzymes, such as fatty acid amide hydrolase (FAAH). The CB1 signaling increases food intake and intestinal permeability, while CB2 signaling might develop anti-inflammatory effects. Oleoylethanolamide (OEA) and palmitoylethanolamide (PEA) are endocannabinoid-like compounds responsible for activating other receptors instead CB1 and CB2, as well as affecting endocannabinoid signaling by FAAH inhibition. PEA and OEA have been associated with anti-inflammatory effects and weight loss, respectively. Maternal high-fat diet (HFD) over activates CB1 in the brain and white adipose tissue (WAT) throughout life of offspring, which develop obesity. It is unexplored the effect of maternal HFD on the ECS of the small intestine of rat offspring associated with the fecal levels of PEA and OEA, whose increased excretion could be associated with intestinal and systemic disorders.