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Diabetes Obes Metab. 2015 Jun;17(6):541-5. doi: 10.1111/dom.12452. Epub 2015 Mar 25.

Imeglimin increases glucose-dependent insulin secretion and improves β-cell function in patients with type 2 diabetes.

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Metabolic (Modeling) Unit, Institute of Biomedical Engineering, Padova, Italy.



To assess the glucose-stimulated insulin secretion effect of imeglimin in patients with type 2 diabetes.


We conducted a double-blind, randomized, placebo-controlled study in 33 patients with type 2 diabetes [glycated haemoglobin 6.8 ± 0.1% (51 mmol/mol)], who were drug-naïve or withdrawn from their previous metformin monotherapy for 2 weeks and received imeglimin 1500 mg twice daily or placebo for 1 week. Glucose-stimulated insulin secretion was assessed using a hyperglycaemic clamp. The primary endpoint was insulin secretion as defined by total insulin response [incremental area under the curve (iAUC)0-45 min ] and insulin secretion rate (ISR) calculated from C-peptide deconvolution. β-cell glucose sensitivity at steady state (second phase: 25-45 min), hepatic insulin extraction and insulin clearance were also calculated.


Imeglimin treatment for 7 days raised the insulin secretory response to glucose by +112% (iAUC0-45 , p = 0.035), first-phase ISR by +110% (p = 0.034) and second-phase ISR by +29% (p = 0.031). Imeglimin improved β-cell glucose sensitivity by +36% (p = 0.034) and tended to decrease hepatic insulin extraction (-13%; p = 0.056). Imeglimin did not affect glucagon secretion.


In patients with type 2 diabetes, imeglimin improves β-cell function, which may contribute to the glucose-lowering effect observed with imeglimin in clinical trials.


Glucose-lowering drug; beta cell; clinical trial; insulin secretion; randomised trial; type 2 diabetes

[Indexed for MEDLINE]

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