Cholecystokinin and serotonin receptors in the regulation of fat-induced satiety in rats
Cholecystokinin and serotonin receptors in the regulation of fat-induced satiety in rats
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DOI：
10.1152/ajpregu.1999.276.2.r429
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发表时间：
1999-02-01
影响因子：
2.8
通讯作者：
Schneeman, BO
中科院分区：
文献类型：
--
作者：
Burton-Freeman, B;Gietzen, DW;Schneeman, BO
本研究探讨了内源性CCK与5-羟色胺（5-HT）在脂肪诱导饱腹感中的关系。十二指肠插管的雄性Wistar大鼠适应每天进食6小时，同时接受生理盐水或两种等热量溶液（10毫升，1千卡/毫升，0.45毫升/分钟）中的一种的输注，不同的脂肪和碳水化合物含量（20%或80%的能量来自脂肪）。大鼠在食物呈现后10分钟注射。饱腹/饱腹反应是通过测量餐量（MS）、餐间间隔（IMI）和总食物摄入量（TFI）来确定的。与生理盐水相比，输注任一脂肪溶液均可降低MS；然而，与生理盐水和20%脂肪输注相比，80%脂肪输注降低了TFI并延长了IMI。在80%脂肪输注CCK和/或5-HT3受体拮抗剂Devazepide （Dev）和Tropisetron （Trop）之前，研究CCK和5-HT参与脂肪诱导的饱腹感。在20%脂肪灌注液中加入CCK释放剂胰蛋白酶抑制剂（TI）以提高饱腹感。单独用Dev或Trop预处理可以减弱80%溶液对IMI的抑制作用，而对MS和TFI的抑制作用的逆转仅对Dev提供的剂量敏感。两种拮抗剂一起完全阻断了80%脂肪灌注对所有喂养变量的饱腹效应。在20%脂肪输注中加入TI延长了IMI，但对MS或TFI没有影响。这些结果为内源性CCK和5-HT参与肠道对脂肪的饱腹反应提供了证据。
The present study investigated the relationship between endogenous CCK and serotonin (5-HT) in fat-induced satiety. Male Wistar rats with duodenal cannulas were adapted to eating 6 h/day along with receiving an infusion of saline or one of two isocaloric solutions (10 ml, 1 kcal/ml, 0.45 ml/min) varying in fat and carbohydrate content (20 or 80% energy from fat). Rats were infused 10 min after food presentation. The satiation/satiety response was determined from measures of meal size (MS), intermeal interval (IMI), and total food intake (TFI). Infusion with either fat solution reduced MS compared with saline; however, the 80% fat infusate reduced TFI and lengthened the IMI compared with saline and the 20% fat infusate. CCK and 5-HT involvement in fat-induced satiety was investigated by preceding the 80% fat infusate with CCK and/or 5-HT3 receptor antagonists Devazepide (Dev) and Tropisetron (Trop). A CCK releaser, trypsin inhibitor (TI), was added to the 20% fat infusate to enhance satiety. Pretreatment with Dev or Trop alone attenuated the inhibitory effects of the 80% solution on IMI, whereas reversal of the inhibitory effects on MS and TFI were sensitive only to Dev at the doses provided. Both antagonists together completely blocked the satiating effects of the 80% fat infusate on all feeding variables measured. Addition of TI to the 20% fat infusate lengthened the IMI but did not affect MS or TFI. These results provide evidence for the participation of both endogenous CCK and 5-HT in the satiety response to fat in the intestine.