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首页> 外文期刊>Diabetes care >Effects of Sustained Treatment With Lixisenatide on Gastric Emptying and Postprandial Glucose Metabolism in Type 2 Diabetes: A Randomized Controlled Trial
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Effects of Sustained Treatment With Lixisenatide on Gastric Emptying and Postprandial Glucose Metabolism in Type 2 Diabetes: A Randomized Controlled Trial

机译：Lixisenatide对2型糖尿病胃排空和后葡萄糖代谢的持续治疗效果：随机对照试验

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OBJECTIVE Tachyphylaxis for slowing of gastric emptying is seen with continuous exposure to glucagon-like peptide 1 (GLP-1). We therefore aimed to establish whether prolonged use of a "short-acting" GLP-1 receptor agonist, lixisenatide, achieves sustained slowing of gastric emptying and reduction in postprandial glycemia. RESEARCH DESIGN AND METHODS A total of 30 patients with metformin-treated type 2 diabetes underwent assessment of gastric emptying (scintigraphy) and glucose metabolism (dual tracer technique) after a 75-g glucose drink, before and after 8 weeks' treatment with lixisenatide (20 mu g subcutaneously daily) or placebo, in a double-blind randomized parallel design. RESULTS Gastric retention of the glucose drink was markedly increased after lixisenatide versus placebo (ratio of adjusted geometric means for area under the curve [AUC] over 240 min of 2.19 [95% CI 1.82, 2.64],P< 0.001), associated with substantial reductions in the rate of systemic appearance of oral glucose (P< 0.001) and incremental AUC for blood glucose (P< 0.001). Lixisenatide suppressed both glucagon (P= 0.003) and insulin (P= 0.032), but not endogenous glucose production, over 120 min after oral glucose intake. Postprandial glucose lowering over 240 min was strongly related to the magnitude of slowing of gastric emptying by lixisenatide (r= -0.74,P= 0.002) and to the baseline rate of emptying (r= 0.52,P= 0.048) but unrelated to beta-cell function (assessed by beta-cell glucose sensitivity). CONCLUSIONS Eight weeks' treatment with lixisenatide is associated with sustained slowing of gastric emptying and marked reductions in postprandial glycemia and appearance of ingested glucose. Short-acting GLP-1 receptor agonists therefore potentially represent an effective long-term therapy for specifically targeting postprandial glucose excursions.
机译：胃排空减慢目的快速耐受被认为是与连续暴露于胰高血糖素样肽1（GLP-1）。因此，我们的目的是确定是否长时间使用一个“短效” GLP-1受体激动剂，利西拉，实现持续餐后血糖胃排空和减少的放缓。研究设计和方法总共30例二甲双胍治疗的2型糖尿病的胃排空（显像）和葡萄糖代谢（双示踪技术）的例行评估75克葡萄糖饮料后，前，后8周与利西拉处理（ 20亩克，每日皮下）或安慰剂，在一个随机双盲平行设计。结果的葡萄糖饮料的胃中的滞留后利西拉与安慰剂显着增加（调节几何平均值为曲线下面积比[AUC]超过2.19 [95％CI 1.82，2.64]，P <0.001 240分钟）中，用大量的相关联的削减口服葡萄糖的全身外观（P <0.001）和用于血糖增量AUC（P <0.001）的速率。利西拉抑制胰高血糖素都（P = 0.003）和胰岛素（P = 0.032），但不内源性葡萄糖生成，经后口服葡萄糖摄入120分钟。餐后血糖降低了超过240分钟强烈涉及由利西拉减慢胃排空的幅度（R = -0.74，P = 0.002），并排空的基线率（r = 0.52，P = 0.048），但不相关的β-葡细胞的功能（由β细胞的葡萄糖敏感性的评估）。结论八周与利西拉治疗与胃排空减慢持续和餐后血糖的显着减少及血糖摄入的出现有关。短效因此GLP-1受体激动剂的潜在代表一个有效的长期治疗对于特异性靶向餐后血糖波动。

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