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内源性阿片肽参与调节小鼠脂肪测试餐的胃排空。

Involvement of endogenous opiates in regulation of gastric emptying of fat test meals in mice.

作者信息

Fioramonti J, Fargeas M J, Bueno L

机构信息

Department of Pharmacology, Institut National de la Recherche Agronomique, Toulouse, France.

出版信息

Am J Physiol. 1988 Aug;255(2 Pt 1):G158-61. doi: 10.1152/ajpgi.1988.255.2.G158.

Abstract

The role of endogenous opioids and cholecystokinin (CCK) in gastric emptying was investigated in mice killed 30 min after gavage with 51Cr-radiolabeled liquid meals. The meals consisted of 0.5 ml of milk or one of five synthetic meals containing arabic gum, glucose and/or arachis oil and/or casein. Naloxone (0.1 mg/kg sc) significantly (P less than 0.01) accelerated gastric emptying of milk and meals containing fat but did not modify gastric emptying of nonfat meals. The CCK antagonist asperlicin (0.1 mg/kg ip) increased by 25% gastric emptying of milk. The gastric emptying of meals containing glucose and casein but not fat was reduced after administration of the COOH-terminal octapeptide of cholecystokinin (CCK-8, 4 micrograms/kg ip). This decrease was antagonized by both asperlicin (10 mg/kg ip) and naloxone (0.1 mg/kg sc). Intracerebroventricular (icv) administration of an opiate antagonist that poorly crosses the blood-brain barrier, methyl levallorphan (10 micrograms/kg), did not modify gastric emptying of milk but accelerated it when peripherally administered (0.1 mg/kg sc). Similarly, asperlicin (icv) administered at a dose of 1 mg/kg did not affect milk emptying. These results indicate that endogenous opiates are involved at peripheral levels in the regulation of gastric emptying of fat meals only and that such regulation involves release of CCK.

摘要

在用51Cr放射性标记的流食灌胃30分钟后处死的小鼠中,研究了内源性阿片类物质和胆囊收缩素(CCK)在胃排空中的作用。流食由0.5毫升牛奶或五种含阿拉伯胶、葡萄糖和/或花生油和/或酪蛋白的合成流食之一组成。纳洛酮(0.1毫克/千克,皮下注射)显著(P<0.01)加速了牛奶和含脂肪流食的胃排空,但未改变无脂流食的胃排空。CCK拮抗剂阿哌利辛(0.1毫克/千克,腹腔注射)使牛奶的胃排空增加了25%。给予胆囊收缩素的羧基末端八肽(CCK-8,4微克/千克,腹腔注射)后,含葡萄糖和酪蛋白但不含脂肪的流食的胃排空减少。阿哌利辛(10毫克/千克,腹腔注射)和纳洛酮(0.1毫克/千克,皮下注射)均拮抗了这种减少。脑室注射不易透过血脑屏障的阿片拮抗剂左甲拉啡烷(10微克/千克)未改变牛奶的胃排空,但外周给药(0.1毫克/千克,皮下注射)时则加速了胃排空。同样,以1毫克/千克的剂量脑室注射阿哌利辛不影响牛奶排空。这些结果表明,内源性阿片类物质仅在外周水平参与脂肪流食胃排空的调节,且这种调节涉及CCK的释放。

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