• P Janssen, H Pottel, R Vos, and J Tack.
• Department of Internal Medicine, University Hospital Gasthuisberg, University of Leuven, Belgium. pieter.janssen@med.kuleuven.be
• Aliment. Pharmacol. Ther. 2011 Mar 1;33(5):607-14.

BackgroundThe centrally acting mu-opioid receptor antagonist naloxone inhibits meal-induced gastric accommodation.AimTo study the role of peripheral mu-opioid receptors in the regulation of gastric tone and food intake by comparing the effects of naloxone with the peripherally restricted mu-opioid receptor antagonist methylnaltrexone.MethodsMethylnaltrexone (12 mg s.c.), naloxone (20 μg/kg/h intravenous infusion after 0.4 mg bolus) and placebo were studied in 23 healthy volunteers. Gastric volume was recorded using an intragastric bag held at constant pressure connected to a barostat, with administration of a nutrient drink after 30 min. Pressure in the stomach was measured during intragastric nutrient drink infusion until the volunteers scored maximal satiation.ResultsMethylnaltrexone inhibited significantly the volume increase after food intake as assessed with the barostat (P < 0.01). During nutrient drink infusion the intragastric pressure significantly decreased as compared with the preprandial pressure after placebo treatment. Both methylnaltrexone and naloxone significantly inhibited this intragastric pressure decrease (P < 0.001 and P < 0.05, respectively). Volunteers scored maximal satiation after 979 ± 96, 958 ± 84 and 1124 ± 107 mL nutrient drink infused (for naloxone, methylnaltrexone and placebo treatment, respectively; P < 0.05).ConclusionsThese results indicate that endogenous opioids mediate gastric accommodation and satiation via peripheral mu-opioid receptors. Effects were less pronounced after naloxone treatment, which indicates that centrally involved mu-opioid receptors mediate an opposing effect.© 2010 Blackwell Publishing Ltd.

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