Intestinal nutrients elicit satiation through concomitant activation of CCK₁ and 5-HT₃ receptors

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• 作者：David M. Savastano ; Mihai Covasa
• 关键词：Food intake ; Satiety ; Gut peptides ; Brain gut interaction
• 刊名：Physiology and Behavior
• 出版年：2007
• 出版时间：22 October 2007
• 年：2007
• 卷：92
• 期：3
• 页码：434-442
• 全文大小：246 K

文摘

Previous studies demonstrate that cholecystokinin type-1 (CCK₁) and serotonin type-3 (5-HT₃) dependent pathways are independently involved in intestinal nutrient-induced meal termination. In the current study, we employed selective antagonists to investigate the relative contribution of CCK₁ and 5-HT₃ receptors in mediating the anorexia produced by duodenal infusion of Polycose or Intralipid in rats. Combined administration of 1 mg/kg ondansetron (Ond) and 1 mg/kg devazepide (Dev) reversed 132 mM Polycose-induced suppression to the level of control intake and significantly attenuated 263 mM Polycose-induced suppression greater than either antagonist alone. Similar results were observed when subthreshold doses of Ond (500 μg/kg) and Dev (5 μg/kg) were co-administered prior to 263 mM Polycose infusion. Suppression of intake resulting from 130 mM Intralipid was reversed to the level of control when Ond and Dev were co-administered at both independent effective doses (1 mg/kg each) and subthreshold doses (500 μg/kg and 5 μg/kg, respectively). Finally, combined administration of the antagonists increased sucrose intakes beyond intakes following control or treatment with either antagonist alone when rats were infused with saline. These data demonstrate that intestinal carbohydrates and lipids inhibit food intake through simultaneous CCK₁ and 5-HT₃ receptor activation and that these receptors appear to completely mediate the Intralipid-induced suppression of intake.