https://eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=pubmed&id=21543633&retmode=xml&tool=Litmetric&email=readroberts32@gmail.com&api_key=61f08fa0b96a73de8c900d749fcb997acc09 215436332011090820211020
1522-149030112011JulAmerican journal of physiology. Regulatory, integrative and comparative physiologyAm J Physiol Regul Integr Comp Physiolmu-Opioid receptor stimulation in the nucleus accumbens elevates fatty tastant intake by increasing palatability and suppressing satiety signals.R244R254R244-5410.1152/ajpregu.00406.2010Infusion of a μ-opioid receptor (MOR) agonist into the nucleus accumbens (NAcc) drives voracious food intake, an effect hypothesized to occur through increased tastant palatability. While intake of many palatable foods is elevated by MOR stimulation, this manipulation has a preferential effect on fatty food ingestion. Consumption of high-fat foods is increased by NAcc MOR stimulation even in rats that prefer a carbohydrate-rich alternative under baseline conditions. This suggests that NAcc MOR stimulation may not simply potentiate palatability signals and raises the possibility that mechanisms mediating fat intake may be distinct from those underlying intake of other tastants. The present study was conducted to investigate the physiological mechanisms underlying the effects of NAcc MOR stimulation on fatty food intake. In experiment 1, we analyzed lick microstructure in rats ingesting Intralipid to identify the changes underlying feeding induced by infusion of a MOR-specific agonist into the NAcc. MOR stimulation in the NAcc core, but not shell, increased burst duration and first-minute licks, while simultaneously increasing the rate and duration of Intralipid ingestion. These results suggest that MOR activation in the core increases Intralipid palatability and attenuates inhibitory postingestive feedback. In experiment 2, we measured the effects of MOR stimulation in the NAcc core on consumption of nonnutritive olestra. A MOR-specific agonist dose dependently increased olestra intake, demonstrating that caloric signaling is not required for hyperphagia induced by NAcc MOR stimulation. Feeding induced by drug infusion in both experiments 1 and 2 was blocked by a MOR antagonist. In experiment 3, we determined whether MOR activation in the NAcc core could attenuate satiety-related signaling caused by infusion of the melanocortin agonist MTII into the third ventricle. Suppression of intake caused by MTII was reversed by MOR stimulation. Together, our results suggest that MOR stimulation in the NAcc core elevates fatty food intake through palatability mechanisms dependent on orosensory cues and suppression of satiety signals inhibiting food intake.KatsuuraYoshihiroYDepartment of Physiology, University of Utah School of Medicine, Salt Lake City, Utah, USA.HeckmannJennifer AJATahaSharif ASAengR21 MH082325MHNIMH NIH HHSUnited StatesMH-082325MHNIMH NIH HHSUnited StatesJournal ArticleResearch Support, N.I.H., ExtramuralResearch Support, Non-U.S. Gov't20110504
United StatesAm J Physiol Regul Integr Comp Physiol1009012300363-61190Analgesics, Opioid0Dietary Fats0Fatty Acids0Melanocortins0Receptors, Opioid, mu100929-53-1Enkephalin, Ala(2)-MePhe(4)-Gly(5)-57-50-1Sucrose6742Y30KGKsucrose polyesterIMAnalgesics, Opioidadverse effectsAnimalsBehavior, AnimalphysiologyDietary FatsmetabolismEatingphysiologyEnkephalin, Ala(2)-MePhe(4)-Gly(5)-adverse effectsFatty AcidsmetabolismFeeding BehaviorphysiologyHyperphagiachemically inducedphysiopathologyMaleMelanocortinsphysiologyModels, AnimalNucleus AccumbensphysiologyRatsRats, Sprague-DawleyReceptors, Opioid, muphysiologySatiety ResponsephysiologySignal TransductionphysiologySucroseanalogs & derivativesmetabolismTaste Perceptionphysiology201156602011566020119960201271ppublish21543633PMC312987210.1152/ajpregu.00406.2010ajpregu.00406.2010Baird JP, St John SJ, Nguyen EA. 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