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The dipeptidyl peptidase‐4 inhibitor linagliptin lowers postprandial glucose and improves measures of β ‐cell function in type 2 diabetes
Author(s) -
Heise T.,
Larbig M.,
Patel S.,
Seck T.,
Hehnke U.,
Woerle H.J.,
Dugi K.
Publication year - 2014
Publication title -
diabetes, obesity and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.445
H-Index - 128
eISSN - 1463-1326
pISSN - 1462-8902
DOI - 10.1111/dom.12312
Subject(s) - linagliptin , postprandial , dipeptidyl peptidase 4 inhibitor , placebo , medicine , diabetes mellitus , type 2 diabetes , dipeptidyl peptidase 4 , endocrinology , gastroenterology , pharmacology , pathology , alternative medicine
Progressive deterioration of pancreatic β‐cell function in patients with type 2 diabetes mellitus ( T2DM ) contributes to worsening of hyperglycaemia. To investigate the effects of the dipeptidyl peptidase‐4 inhibitor linagliptin on β‐cell function parameters, a pooled analysis of six randomized, 24‐week, placebo‐controlled, phase 3 trials of 5 mg of linagliptin daily was performed in 2701 patients with T2DM (linagliptin, n = 1905; placebo, n = 796). At week 24, observed improvements in HbA1c , fasting plasma glucose, and 2‐h postprandial glucose were significantly greater for linagliptin than placebo (all p < 0.0001). Homeostasis model assessment ( HOMA )‐%β, as a surrogate marker of fasting β‐cell function, was significantly improved with linagliptin, and did not change with placebo (placebo‐adjusted mean ± s.e. change for linagliptin: 16.5 ± 4.6 ( mU /l)/(mmol/l); p = 0.0003). Further study is required to determine if the significant improvement in HOMA ‐%β with linagliptin will translate into long‐term improvements in β‐cell function.