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脂肪酸链长度决定胆囊收缩素的分泌及其对人体胃动力的影响。

Fatty acid chain length determines cholecystokinin secretion and effect on human gastric motility.

作者信息

McLaughlin J, Grazia Lucà M, Jones M N, D'Amato M, Dockray G J, Thompson D G

机构信息

Department of Medicine, University of Manchester, Manchester, England.

出版信息

Gastroenterology. 1999 Jan;116(1):46-53. doi: 10.1016/s0016-5085(99)70227-1.

Abstract

BACKGROUND & AIMS: Fatty acids induce cholecystokinin (CCK) secretion and modify gastric motility, but the chain length requirements for these effects are not known. Nor is it clear whether the effects of fatty acids on gastric motility in humans are CCK mediated or directly exerted. The aim of this study was to determine the role of fatty acyl chain length in CCK secretion and in influencing gastric motility.

METHODS

Fatty acids were infused into the upper gut in healthy volunteers; plasma CCK was determined by radioimmunoassay. Effects of fatty acids on antral contractility were determined by percutaneous ultrasonography; effects on proximal gastric tone were studied during fundal distention.

RESULTS

Plasma CCK concentration was consistently and similarly elevated by fatty acids with a chain of 12 carbon atoms or longer, whereas those of 11 or fewer carbon atoms failed to increase plasma CCK. A 12-carbon but not a 10-carbon-long chain fatty acid reduced antral contractile amplitude, an effect that was abolished by loxiglumide (a specific CCK-A receptor antagonist). The 12-carbon fatty acid also reduced proximal gastric tone more than the 10-carbon fatty acid.

CONCLUSIONS

A highly specific, chain length-sensitive fatty acid recognition system exists in the proximal gut mediating CCK secretion and gastric motility. An additional, probably CCK-independent, effect of fatty acid also regulates proximal gastric tone.

摘要

背景与目的

脂肪酸可诱导胆囊收缩素(CCK)分泌并改变胃动力,但这些作用对脂肪酸链长度的要求尚不清楚。脂肪酸对人体胃动力的影响是由CCK介导还是直接发挥作用也不明确。本研究的目的是确定脂肪酰链长度在CCK分泌及影响胃动力方面的作用。

方法

将脂肪酸注入健康志愿者的上消化道;采用放射免疫分析法测定血浆CCK。通过经皮超声检查确定脂肪酸对胃窦收缩性的影响;在胃底扩张时研究其对胃近端张力的影响。

结果

含12个或更多碳原子链的脂肪酸可使血浆CCK浓度持续且相似地升高,而含11个或更少碳原子的脂肪酸则不能使血浆CCK升高。含12个碳原子而非10个碳原子的长链脂肪酸可降低胃窦收缩幅度,洛西丁胺(一种特异性CCK-A受体拮抗剂)可消除该作用。含12个碳原子的脂肪酸比含10个碳原子的脂肪酸更能降低胃近端张力。

结论

近端肠道中存在一种高度特异性、对链长度敏感的脂肪酸识别系统,介导CCK分泌和胃动力。脂肪酸还有一种可能不依赖CCK的额外作用,也可调节胃近端张力。

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