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Sitagliptin improves beta‐cell function in patients with acute coronary syndromes and newly diagnosed glucose abnormalities–the BEGAMI study
Author(s) -
Hage C.,
Brismar K.,
Efendic S.,
Lundman P.,
Rydén L.,
Mellbin L.
Publication year - 2013
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1111/joim.12032
Subject(s) - sitagliptin , medicine , placebo , sitagliptin phosphate , impaired glucose tolerance , endocrinology , diabetes mellitus , myocardial infarction , dipeptidyl peptidase 4 inhibitor , acute coronary syndrome , metformin , unstable angina , type 2 diabetes , gastroenterology , cardiology , pathology , alternative medicine
Background Newly detected impaired glucose tolerance ( IGT ) or type 2 diabetes mellitus (T2 DM ) 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. Methods Acute coronary syndrome ACS patients with IGT or T2 DM ( 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 = ΔInsulin 30 /ΔGlucose 30 ), derived from an OGTT , and acute insulin response to glucose ( AIR g) assessed by a frequently sampled intravenous glucose tolerance test. Results The IGI and AIR g 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 AIR g 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. Conclusion Sitagliptin improved beta‐cell function and glucose perturbations in patients with ACS and newly diagnosed glucose disturbances.