Effects of Sustained Treatment With Lixisenatide on Gastric Emptying and Postprandial Glucose Metabolism in Type 2 Diabetes: A Randomized Controlled Trial

May 31, 2020Diabetes care

Lixisenatide’s long-term effects on stomach emptying and blood sugar after meals in type 2 diabetes

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Abstract

Gastric retention of a glucose drink increased by 2.19 times after treatment with lixisenatide compared to placebo.

Lixisenatide treatment led to significant reductions in the rate of systemic appearance of oral glucose.
Postprandial blood glucose levels showed substantial decreases following lixisenatide administration.
Lixisenatide suppressed glucagon and insulin levels after glucose intake, without affecting endogenous glucose production.
The extent of postprandial glucose reduction was closely linked to the degree of gastric emptying slowing caused by lixisenatide.
The baseline rate of gastric emptying also played a role in determining postprandial glucose outcomes.

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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 μg 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],< 0.001), associated with substantial reductions in the rate of systemic appearance of oral glucose (< 0.001) and incremental AUC for blood glucose (< 0.001). Lixisenatide suppressed both glucagon (= 0.003) and insulin (= 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 (= -0.74,= 0.002) and to the baseline rate of emptying (= 0.52,= 0.048) but unrelated to β-cell function (assessed by β-cell glucose sensitivity). P P P P P r P r P

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.

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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

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