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首页> 外文期刊>Diabetes care >Effects of intraduodenal glutamine on incretin hormone and insulin release, the glycemic response to an intraduodenal glucose infusion, and antropyloroduodenal motility in health and type 2 diabetes.
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Effects of intraduodenal glutamine on incretin hormone and insulin release, the glycemic response to an intraduodenal glucose infusion, and antropyloroduodenal motility in health and type 2 diabetes.

机译:谷氨酰胺对胰蛋白激素和胰岛素释放,对体内葡萄糖输注的血糖反应,健康和2型糖尿病患者血糖反应的影响。

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OBJECTIVE Glutamine reduces postprandial glycemia when given before oral glucose. We evaluated whether this is mediated by stimulation of insulin and/or slowing of gastric emptying. RESEARCH DESIGN AND METHODS Ten healthy subjects were studied during intraduodenal (ID) infusion of glutamine (7.5 or 15 g) or saline over 30 min, followed by glucose (75 g over 100 min), while recording antropyloroduodenal pressures. Ten patients with type 2 diabetes mellitus (T2DM) were also studied with 15 g glutamine or saline. RESULTS ID glutamine stimulated glucagon-like peptide 1 (GLP-1; healthy: P < 0.05; T2DM: P < 0.05), glucose-dependent insulinotropic polypeptide (GIP; P = 0.098; P < 0.05), glucagon (P < 0.01; P < 0.001), insulin (P = 0.05; P < 0.01), and phasic pyloric pressures (P < 0.05; P < 0.05), but did not lower blood glucose (P = 0.077; P = 0.5). CONCLUSIONS Glutamine does not lower glycemia after ID glucose, despite stimulating GLP-1, GIP, and insulin, probably due to increased glucagon. Its capacity for pyloric stimulation suggests that delayed gastric emptying is a major mechanism for lowering glycemia when glutamine is given before oral glucose.
机译:目标谷氨酰胺在口服葡萄糖前给予后糖血症。我们评估了这是否通过刺激胰岛素和/或胃排空减慢来介导。研究设计和方法在30分钟内抑制谷氨酰胺(7.5或15g)或盐水中的肺结核(ID),然后进行葡萄糖(超过100分钟),同时记录葡萄糖(75克超过100分钟)。还用15g谷氨酰胺或盐水研究了10型糖尿病患者的2型糖尿病(T2DM)。结果ID谷氨酰胺刺激胰高血糖素样肽1(GLP-1;健康:P <0.05; T2DM:P <0.05),葡萄糖依赖性胰岛素多肽(GIP; P = 0.098; P <0.05),胰高血糖素(P <0.01; P <0.001),胰岛素(P = 0.05; P <0.01),相位幽门压力(P <0.05; P <0.05),但没有降低血糖(P = 0.077; P = 0.5)。结论谷氨酰胺在ID葡萄糖后不会降低糖血症,尽管刺激GLP-1,GIP和胰岛素,可能是由于胰高血糖素增加。它的幽门刺激能力表明,延迟胃排空是在口服葡萄糖前给予谷氨酰胺时降低糖血症的主要机制。

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