Abstract
Oleoylethanolamide (OEA) is an endogenous lipid mediator that inhibits feeding in rats and mice by activating the nuclear receptor peroxisome proliferator-activated receptor-alpha (PPAR-alpha). In rodents, intestinal OEA levels increase about threefold upon refeeding, a response that may contribute to the induction of between-meal satiety. Here, we examined whether feeding-induced OEA mobilization also occurs in Burmese pythons (Python molurus), a species of ambush-hunting snakes that consume huge meals after months of fasting and undergo massive feeding-dependent changes in gastrointestinal hormonal release and gut morphology. Using liquid chromatography/mass spectrometry (LC/MS), we measured OEA levels in the gastrointestinal tract of fasted (28 days) and fed (48 h after feeding) pythons. We observed a nearly 300-fold increase in OEA levels in the small intestine of fed compared with fasted animals (322 +/- 121 vs. 1 +/- 1 pmol/mg protein, n = 3-4). In situ OEA biosynthesis was suggested by the concomitant increase of N-acyl phosphatidylethanolamine species that serve as potential biosynthetic precursors for OEA. Furthermore, we observed a concomitant increase in saturated, mono- and diunsaturated, but not polyunsaturated fatty-acid ethanolamides (FAE) in the small intestine of fed pythons. The identification of OEA and other FAEs in the gastrointestinal tract of Python molurus suggests that this class of lipid messengers may be widespread among vertebrate groups and may represent an evolutionarily ancient means of regulating energy intake.
Highlights
THE GASTROINTESTINAL TRACT plays a pivotal role in the regulation of vertebrate feeding and digestion, controlling multiple aspects of this process through both neuronal and humoral mechanisms
Oleoylethanolamide (OEA)—the amide of oleic acid and ethanolamine—is synthesized in a variety of rodent tissues, including the small intestine, where its levels decrease during food deprivation and increase upon refeeding [24]
These findings suggest that OEA is a lipid mediator produced in the small intestine, which regulates feeding behavior by activating local PPAR-␣
Summary
THE GASTROINTESTINAL TRACT plays a pivotal role in the regulation of vertebrate feeding and digestion, controlling multiple aspects of this process through both neuronal and humoral mechanisms. Among the humoral signals released by the gut, peptides, such as cholecystokinin, glucagon-like peptide-1, and ghrelin have attracted the most attention [4], but recent evidence suggests that lipid messengers are involved [7, 18] One such messenger, oleoylethanolamide (OEA)—the amide of oleic acid and ethanolamine—is synthesized in a variety of rodent tissues, including the small intestine, where its levels decrease during food deprivation and increase upon refeeding [24]. Mutant mice in which the PPAR-␣ gene has been deleted by homologous recombination (PPAR-␣Ϫ/Ϫ mice) do not respond to OEA or synthetic PPAR-␣ agonists, they retain normal anorexiant responses to CCK octapeptide and fenfluramine [10] Together, these findings suggest that OEA is a lipid mediator produced in the small intestine, which regulates feeding behavior by activating local PPAR-␣. We measured levels of OEA and its phospholipid precursors, N-acyl phosphatidylethanolamine (NAPE) [6], in gastrointestinal segments of fasted and fed pythons
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