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在人类中,胆囊收缩素介导了对肠道脂质作出反应的食物摄入量抑制。

Inhibition of food intake in response to intestinal lipid is mediated by cholecystokinin in humans.

作者信息

Matzinger D, Gutzwiller J P, Drewe J, Orban A, Engel R, D'Amato M, Rovati L, Beglinger C

机构信息

Department of Research and Division of Gastroenterology, University Hospital, CH-4031 Basel, Switzerland.

出版信息

Am J Physiol. 1999 Dec;277(6):R1718-24. doi: 10.1152/ajpregu.1999.277.6.R1718.

Abstract

Intraduodenal fat inhibits gastric emptying and exerts early satiation in animals and humans, but it is not clear whether the effects are mediated by cholecystokinin (CCK) in humans. Here, we tested whether CCK-A receptors mediate the inhibition of fat on food intake. Two sequential, double-blind, crossover studies were performed in 24 male subjects. First, subjects received either intraduodenal fat or saline together with a preload of either water or banana shake. Second, 12 subjects received either intraduodenal fat or saline perfusion plus a concomitant infusion of saline or loxiglumide, a specific CCK-A receptor antagonist, together with a preload of banana shake. In both studies, subjects were free to eat and drink as much as they wished. Fat induced a reduction in calorie intake (P < 0.05) compared with controls. Furthermore, a decrease in hunger feelings was observed. Infusion of loxiglumide abolished the effects of fat. Duodenal fat interacts with an appetizer to modulate energy intake in humans. This effect is mediated by CCK-A receptors.

摘要

十二指肠内脂肪可抑制胃排空,并在动物和人类中产生早期饱腹感,但在人类中,其作用是否由胆囊收缩素(CCK)介导尚不清楚。在此,我们测试了CCK-A受体是否介导脂肪对食物摄入的抑制作用。对24名男性受试者进行了两项连续的双盲交叉研究。首先,受试者接受十二指肠内脂肪或生理盐水,并同时给予水或香蕉奶昔作为预负荷。其次,12名受试者接受十二指肠内脂肪或生理盐水灌注,并同时输注生理盐水或CCK-A受体特异性拮抗剂洛西肽,同时给予香蕉奶昔作为预负荷。在两项研究中,受试者可自由饮食。与对照组相比,脂肪导致热量摄入减少(P<0.05)。此外,还观察到饥饿感下降。输注洛西肽消除了脂肪的作用。十二指肠内脂肪与开胃菜相互作用,调节人类的能量摄入。这种作用由CCK-A受体介导。

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