Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P21554 (cannabinoid receptor)
 3,582 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

GPR55 is a seven transmembrane G protein-coupled receptor and was originally identified as a putative third cannabinoid receptor. Recently, lysophosphatidylinositol (LPI) was reported to be a GPR55 ligand. Stimulation of GPR55 by LPI activates G(12/13) and G(q/11) proteins, induces phosphorylation of the extracellular signal-regulated kinase and increases intracellular calcium concentration. Lysophospholipids are molecularly quite diverse across species and tissues. A recent report showed that the predominant fatty acyl moiety of LPI in rat brain is stearic acid followed by arachidonic acid. The biological activity of arachidonic acid-containing LPI species towards GPR55 was shown to be markedly higher than that of LPI species containing other fatty acyl groups, suggesting that 2-arachidonolyl LPI is the most likely natural ligand of GPR55.
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PMID:What is the natural ligand of GPR55? 2132 83

Dietary fat exerts a potent stimulatory effect on feeding. This effect is mediated, at least in part, by a cephalic mechanism that involves recruitment of the vagus nerve and subsequent activation of endocannabinoid signaling in the gut. Here, we used a sham-feeding protocol in rats to identify fatty-acid constituents of dietary fat that might be responsible for triggering small-intestinal endocannabinoid signaling. Sham feeding rats with a corn oil emulsion increased endocannabinoid levels in jejunum, relative to animals that received either mineral oil (which contains no fatty acids) or no oil. Sham-feeding emulsions containing oleic acid (18:1) or linoleic acid (18:2) caused, on average, a nearly 2-fold accumulation of jejunal endocannabinoids, whereas emulsions containing stearic acid (18:0) or linolenic acid (18:3) had no such effect. In a 2-bottle-choice sham-feeding test, rats displayed strong preference for emulsions containing 18:2, which was blocked by pretreatment with the peripherally restricted CB1 cannabinoid receptor antagonists, AM6546 and URB447. Our results suggest that oral exposure to the monoenoic and dienoic fatty acid component of dietary fat selectively initiates endocannabinoid mobilization in the gut, and that this local signaling event is essential for fat preference.
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PMID:Endocannabinoid signaling in the gut mediates preference for dietary unsaturated fats. 2346 97