Endogenous Glucagon-Like Peptide-1 Slows Gastric Emptying in Healthy Subjects, Attenuating Postprandial Glycemia
Endogenous Glucagon-Like Peptide-1 Slows Gastric Emptying in Healthy Subjects, Attenuating Postprandial Glycemia
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DOI：
10.1210/jc.2009-1503
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发表时间：
2010-01-01
影响因子：
5.8
通讯作者：
Horowitz, Michael
中科院分区：
文献类型：
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作者：
Deane, Adam M.;Nguyen, Nam Q.;Horowitz, Michael
前言：胰升糖素样肽-1(GLP-1)在胃排空调节中的作用尚不清楚。本研究旨在探讨内源性GLP-1对健康受试者胃排空、葡萄糖吸收和血糖的影响。方法：10名健康空腹受试者(8名男性，2名女性；48+/-7岁)以随机、双盲、交叉的方式在-30至180分钟内接受特定的GLP-1拮抗剂exendin(9-39)酰胺[ex(9-39)NH2](300pmol/kg.min iv)或安慰剂的治疗。在0min时，吃含有3g 3-邻甲基-D-葡萄糖(3-OMG)的土豆泥(类似于2600kJ)，并用20MBq(99M)的氚-硫胶标记。结果：EX(9-39)NH2促进胃排空[T50ex(9-39)NH2，68+/-8min，vs安慰剂，83+/-7min；P<；并增加了对膳食的总体血糖反应[曲线下面积(0-180min)ex(9-39)nH2,1540+/-106mmol.min，与安慰剂相比，1388+/-90mmol.min；P<；0.02]。在60分钟时，EX(9-39)NH2使血糖升高[EX(9-39)NH2，9.9+/-0.5 mmol/L，与安慰剂相比，8.4+/-0.5 mmol/L；P<；0.01]，血浆3-OMG[EX(9-39)NH2，0.25+/-0.01 mmol/L，vs安慰剂，0.21+/-0.01 mmol/L；P<；和血浆胰岛素浓度[ex(9-39)NH2，82+/-13mU/升，与安慰剂比较，59+/-9mU/升；P<；0.05]。血糖和胃排空在受试者内有密切的相关性[如60min时，血糖和胃排空增加(T50)；r=-0.89；P<；0.001]。结论：GLP-1在健康人群中起着减慢胃排空的生理作用，从而影响糖的吸收，从而影响餐后血糖。(临床内分泌代谢酶95：215-221,2010)
Introduction: The role of glucagon-like peptide-1 (GLP-1) in the regulation of gastric emptying is uncertain. The aim of this study was to determine the effects of endogenous GLP-1 on gastric emptying, glucose absorption, and glycemia in health.Methods: Ten healthy fasted subjects (eight males, two females; 48 +/- 7 yr) received the specific GLP-1 antagonist, exendin(9-39) amide [ex(9-39)NH2] (300 pmol/kg.min iv), or placebo, between -30 and 180 min in a randomized, double-blind, crossover fashion. At 0 min, a mashed potato meal (similar to 2600 kJ) containing 3 g 3-ortho-methyl-D-glucose (3-OMG) and labeled with 20 MBq (99m)Technetium-sulphur colloid was eaten. Gastric emptying, including the time taken for 50% of the meal to empty from the stomach (T50), blood glucose, plasma 3-OMG, and plasma insulin were measured.Results: Ex(9-39)NH2 accelerated gastric emptying [T50ex(9-39)NH2, 68 +/- 8 min, vs. placebo, 83 +/- 7 min; P < 0.001] and increased the overall glycemic response to the meal [area under the curve (0-180 min) ex(9-39)NH2, 1540 +/- 106 mmol/liter.min, vs. placebo, 1388 +/- 90 mmol/liter.min; P < 0.02]. At 60 min, ex(9-39)NH2 increased the rise in glycemia [ex(9-39)NH2, 9.9 +/- 0.5 mmol/liter, vs. placebo, 8.4 +/- 0.5 mmol/liter; P < 0.01], plasma 3-OMG [ex(9-39)NH2, 0.25 +/- 0.01 mmol/liter, vs. placebo, 0.21 +/- 0.01 mmol/liter; P < 0.05], and plasma insulin [ex(9-39)NH2, 82 +/- 13 mU/liter, vs. placebo, 59 +/- 9 mU/liter; P < 0.05] concentrations. There was a close within-subject correlation between glycemia and gastric emptying [e. g. at 60 min, the increment in blood glucose and gastric emptying (T50); r = -0.89; P < 0.001].Conclusion: GLP-1 plays a physiological role to slow gastric emptying in health, which impacts on glucose absorption and, hence, postprandial glycemia. (J Clin Endocrinol Metab 95: 215-221, 2010)