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APPETITE, OBESITY, DIGESTION, AND METABOLISM

Serotonin type-3 receptors mediate cholecystokinin-induced satiation through gastric distension

Department of Nutritional Sciences, College of Health and Human Development, The Pennsylvania State University, University Park, Pennsylvania

Submitted 4 January 2006 ; accepted in final form 9 February 2006

We have previously shown that serotonin type-3 (5-HT3) receptors mediate cholecystokinin (CCK)-induced satiation and that this effect is dependent on postoropharyngeal feedback. However, the independent contributions of gastric and intestinal feedback in 5-HT3 receptor mediation of suppression of food intake by CCK have not been determined. Using a sham-feeding preparation combined with intraduodenal sucrose infusion, we show that blockade of 5-HT3 receptors by ondansetron (1 mg/kg ip) had no effect on suppression of sham feeding by intraduodenal 15% sucrose infusion (4 ml/10 min), CCK (2 µg/kg ip) administration, or the combination of the two treatments. In separate experiments consisting of either sham-feeding rats that received gastric distension with the use of a balloon or real-feeding rats whose stomachs were distended using gastric loads of saline after the occlusion of the pylorus, we tested the hypothesis that gastric feedback signals are necessary for activation of 5-HT3 receptors. Ondansetron significantly attenuated suppression of sham sucrose intake after a 10-ml gastric balloon distension (30.5 ± 2.2 vs. 20.2 ± 2.2 ml, respectively) and gastric distension combined with CCK (21.9 ± 1.4 vs. 12.0 ± 1.7 ml, respectively). When intestinal feedback was eliminated in a real-feeding paradigm by closing the pylorus using a cuff preparation, ondansetron attenuated suppression of sucrose intake produced by a 10-ml saline gastric load (6.8 ± 0.7 vs. 4.2 ± 0.4 ml, respectively). Finally, when CCK (1 µg/kg) was administered in combination with a 5-ml saline gastric load in a real-feeding preparation, ondansetron significantly attenuated suppression of sucrose intake by CCK (9.0 ± 0.9 vs. 6.3 ± 0.5 ml, respectively), as well as the enhanced suppression of intake by CCK plus gastric load (6.9 ± 0.6 vs. 4.6 ± 0.5 ml, respectively). These findings demonstrate that CCK-induced activation of 5-HT3 receptors requires gastric, but not intestinal feedback.

food intake; stomach; synergistic

This article has been cited by other articles:

				D. M. Savastano, M. R. Hayes, and M. Covasa Serotonin-type 3 receptors mediate intestinal lipid-induced satiation and Fos-like immunoreactivity in the dorsal hindbrain Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2007; 292(3): R1063 - R1070. [Abstract] [Full Text] [PDF]

				D. Tome From gut nutrient sensing to nutrient perception: a cooperative role involving CCK and 5-HT? Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2007; 292(3): R1061 - R1062. [Full Text] [PDF]

				S. Aja Serotonin-3 receptors in gastric mechanisms of cholecystokinin-induced satiety Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2006; 291(1): R112 - R114. [Full Text] [PDF]