Open AccessEffects of vildagliptin on postprandial markers of bone resorption and calcium homeostasis in recently diagnosed, well‐controlled type 2 diabetes patients *
Author(s) -
BUNCK Mathijs C.,
POELMA Marieke,
EEKHOFF E. Marelise,
SCHWEIZER Anja,
HEINE Robert J.,
NIJPELS Giel,
FOLEY James E.,
DIAMANT Michaela
Publication year - 2012
Publication title -
journal of diabetes
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.949
H-Index - 43
eISSN - 1753-0407
pISSN - 1753-0393
DOI - 10.1111/j.1753-0407.2011.00168.x
Subject(s) - vildagliptin , medicine , endocrinology , bone resorption , bone remodeling , glucose homeostasis , postprandial , diabetes mellitus , type 2 diabetes , n terminal telopeptide , calcium metabolism , calcium , alkaline phosphatase , osteocalcin , insulin resistance , chemistry , biochemistry , enzyme
Background: Bone metabolism is a dynamic process that is influenced by food ingestion. Endogenous incretins have been shown to be important regulators of bone turnover. The aim of the present study was to assess whether a dipeptidylpeptidase (DPP)‐4 inhibitor affects markers of bone resorption and calcium homeostasis. Methods: The present study was a single‐center, double blind, randomized clinical trail. Fifty‐nine drug‐naïve patients with type 2 diabetes (T2D) were randomized to either 1 year treatment with the DPP‐4 inhibitor vildagliptin (100 mg, once daily; n = 29) or placebo ( n = 30). Patients received a standardized breakfast after measurement of serum concentrations of cross‐linked C‐terminal telopeptide (s‐CTx), a bone resorption marker influenced by food intake, before and after 50 weeks treatment. Results: Vildagliptin did not change postprandial s‐CTx concentrations compared with pretreatment levels (between‐group ratio 1.15 ± 0.17; P = 0.320). Fasting serum alkaline phosphatase, calcium, and phosphate were also unaffected y 1 year treatment with vildagliptin. Conclusions: Treatment with vildagliptin for 1 year was not associated with changes in markers of bone resorption and calcium homeostasis in drug‐naïve patients with T2D and mild hyperglycemia.