The dipeptidyl peptidase‐4 inhibitor linagliptin lowers postprandial glucose and improves measures of β‐cell function in type 2 diabetes1. Issue 10 (9th June 2014)

• Record Type: Journal Article
• Authors: Heise, T.; Larbig, M.; Patel, S.; Seck, T.; Hehnke, U.; Woerle, H.‐J.; Dugi, K.
• Is Part Of: Diabetes, obesity & metabolism. Volume 16:Issue 10(2014:Oct.)
• Page Start: 1036
• Page End: 1039
• Publication Date: 2014-06-09
• Subjects: Diabetes -- Periodicals; Obesity -- Periodicals; Metabolism -- Disorders -- Periodicals; Clinical pharmacology -- Periodicals; 616.462
• DOI: 10.1111/dom.12312
• Languages: English
• ISSNs: 1462-8902

Abstract

<abstract abstract-type="main" id="dom12312-abs-0001"> <title> <x xml:space="preserve">Abstract</x> </title> <p id="dom12312-para-0001">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 &lt; 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.</p> </abstract>