Sitagliptin improves beta-cell function in patients with acute coronary syndromes and newly diagnosed glucose abnormalities–the BEGAMI study
Version of Record online: 14 FEB 2013
© 2013 The Association for the Publication of the Journal of Internal Medicine
Journal of Internal Medicine
Volume 273, Issue 4, pages 410–421, April 2013
How to Cite
Department of Medicine, Karolinska Institutet; Department of Molecular Medicine and Surgery, Karolinska Institutet; Department of Clinical Sciences, Karolinska Institutet, Danderyd Hospital, Stockholm, Sweden. Sitagliptin improves beta-cell function in patients with acute coronary syndromes and newly diagnosed glucose abnormalities–the BEGAMI study. J Intern Med 2013; doi: 10.1111/joim.12032, , , , ,
- Issue online: 20 MAR 2013
- Version of Record online: 14 FEB 2013
- Accepted manuscript online: 19 JAN 2013 11:55AM EST
- Swedish Heart and Lung Foundation
- AFA Insurance
- Erling-Persson Family Foundation
- Medical Research Council. Grant Number: 04224
- acute coronary syndrome;
- beta-cell function;
- insulinogenic index;
Newly detected impaired glucose tolerance (IGT) or type 2 diabetes mellitus (T2DM) are common in patients with acute coronary syndrome (ACS; i.e. unstable angina/myocardial infarction) and related to disturbed beta-cell function. The aim of this study is to test the hypothesis that treatment with a dipeptidyl peptidase-4 inhibitor initiated soon after a coronary event improves beta-cell function.
Acute coronary syndromeACS patients with IGT or T2DM (n = 71), screened by oral glucose tolerance test (OGTT) 4–23 days (median 6 days) after hospital admission, were randomly assigned to sitagliptin 100 mg (n = 34) or placebo (n = 37) and treated for a duration of 12 weeks. All patients received lifestyle advice but no glucose-lowering agents other than the study drug. The study end-point was beta-cell function assessed using the insulinogenic index (IGI = ΔInsulin30/ΔGlucose30), derived from an OGTT, and acute insulin response to glucose (AIRg) assessed by a frequently sampled intravenous glucose tolerance test.
The IGI and AIRg did not differ at baseline between the sitagliptin and placebo groups (69.9 vs. 66.4 pmol mmol−1 and 1394 vs. 1106 pmol L−1 min−1 respectively). After 12 weeks, the IGI was 85.0 in the sitagliptin and 58.1 pmol/mmol in the placebo group (P = 0.013) and AIRg was 1909 and 1043 pmol L−1 min−1 (P < 0.0001) in the sitagliptin and placebo groups respectively. Fasting glucose at baseline was 6.1 mmol L−1 in sitagliptin-treated patients and 6.0 mmol L−1 in those who received placebo compared with 5.8 and 5.9 mmol L−1 respectively, after 12 weeks of treatment. Post load glucose metabolism improved in significantly more sitagliptin-treated patients compared with the placebo group (P = 0.003). Sitagliptin was well tolerated.
Sitagliptin improved beta-cell function and glucose perturbations in patients with ACS and newly diagnosed glucose disturbances.