Endocannabinoids selectively enhance sweet taste

摘要: Endocannabinoids such as anandamide [N-arachidonoylethanolamine (AEA)] and 2-arachidonoyl glycerol (2-AG) are known orexigenic mediators that act via CB1 receptors in hypothalamus limbic forebrain to induce appetite stimulate food intake. Circulating endocannabinoid levels inversely correlate with plasma of leptin, an anorexigenic mediator reduces intake by acting on hypothalamic receptors. Recently, taste has been found be a peripheral target leptin. Leptin selectively suppresses sweet responses wild-type mice but not leptin receptor-deficient db/db mice. Here, we show endocannabinoids oppose the action enhancers taste. We administration AEA or 2-AG increases gustatory nerve sweeteners concentration-dependent manner without affecting salty, sour, bitter, umami compounds. The cannabinoids increase behavioral sweet-bitter mixtures electrophysiological receptor cells Mice genetically lacking no enhancement endocannnabinoids at cellular, nerve, levels. In addition, effects diminished AM251, antagonist, AM630, CB2 antagonist. Immunohistochemistry shows expressed type II also express T1r3 component. Taken together, these observations suggest organ is endocannabinoids. Reciprocal regulation reception may contribute their opposing actions play important role regulating energy homeostasis.