PMID- 21543633 OWN - NLM STAT- MEDLINE DCOM- 20110908 LR - 20211020 IS - 1522-1490 (Electronic) IS - 0363-6119 (Print) IS - 0363-6119 (Linking) VI - 301 IP - 1 DP - 2011 Jul TI - mu-Opioid receptor stimulation in the nucleus accumbens elevates fatty tastant intake by increasing palatability and suppressing satiety signals. PG - R244-54 LID - 10.1152/ajpregu.00406.2010 [doi] AB - Infusion of a mu-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. FAU - Katsuura, Yoshihiro AU - Katsuura Y AD - Department of Physiology, University of Utah School of Medicine, Salt Lake City, Utah, USA. FAU - Heckmann, Jennifer A AU - Heckmann JA FAU - Taha, Sharif A AU - Taha SA LA - eng GR - R21 MH082325/MH/NIMH NIH HHS/United States GR - MH-082325/MH/NIMH NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't DEP - 20110504 PL - United States TA - Am J Physiol Regul Integr Comp Physiol JT - American journal of physiology. Regulatory, integrative and comparative physiology JID - 100901230 RN - 0 (Analgesics, Opioid) RN - 0 (Dietary Fats) RN - 0 (Fatty Acids) RN - 0 (Melanocortins) RN - 0 (Receptors, Opioid, mu) RN - 100929-53-1 (Enkephalin, Ala(2)-MePhe(4)-Gly(5)-) RN - 57-50-1 (Sucrose) RN - 6742Y30KGK (sucrose polyester) SB - IM MH - Analgesics, Opioid/adverse effects MH - Animals MH - Behavior, Animal/physiology MH - Dietary Fats/*metabolism MH - Eating/*physiology MH - Enkephalin, Ala(2)-MePhe(4)-Gly(5)-/adverse effects MH - Fatty Acids/metabolism MH - Feeding Behavior/physiology MH - Hyperphagia/chemically induced/physiopathology MH - Male MH - Melanocortins/physiology MH - Models, Animal MH - Nucleus Accumbens/*physiology MH - Rats MH - Rats, Sprague-Dawley MH - Receptors, Opioid, mu/*physiology MH - Satiety Response/*physiology MH - Signal Transduction/*physiology MH - Sucrose/analogs & derivatives/metabolism MH - Taste Perception/*physiology PMC - PMC3129872 EDAT- 2011/05/06 06:00 MHDA- 2011/09/09 06:00 PMCR- 2012/07/01 CRDT- 2011/05/06 06:00 PHST- 2011/05/06 06:00 [entrez] PHST- 2011/05/06 06:00 [pubmed] PHST- 2011/09/09 06:00 [medline] PHST- 2012/07/01 00:00 [pmc-release] AID - ajpregu.00406.2010 [pii] AID - R-00406-2010 [pii] AID - 10.1152/ajpregu.00406.2010 [doi] PST - ppublish SO - Am J Physiol Regul Integr Comp Physiol. 2011 Jul;301(1):R244-54. doi: 10.1152/ajpregu.00406.2010. Epub 2011 May 4.