Literature DB >> 24485397

The dipeptidyl peptidase-4 inhibitor vildagliptin does not affect ex vivo cytokine response and lymphocyte function in patients with type 2 diabetes mellitus.

P C M van Poppel1, M S Gresnigt2, P Smits3, M G Netea2, C J Tack4.   

Abstract

AIMS: The enzyme dipeptidyl peptidase-4 (DPP-4) is a key player in the degradation of incretin hormones that are involved in glucose metabolism. DPP-4 is also expressed on immune cells and is associated with several immunological functions. Some studies have reported increased rates of infections in patients treated with DPP-4 inhibitors. We therefore assessed whether treatment with the DPP-4 inhibitor vildagliptin affected cytokine production and T-cell differentiation.
METHODS: Patients with type 2 diabetes were treated with vildagliptin or an active comparator, acarbose, for four weeks, in a randomized cross-over trial. Blood was sampled at the end of each treatment period and peripheral blood mononuclear cells were isolated and stimulated with a broad spectrum of pattern recognition receptor agonists.
RESULTS: Serum cytokine concentrations and ex vivo cytokine production (both monocyte and T-cell derived) did not differ during treatment with vildagliptin compared to acarbose. Similarly, ex vivo relative upregulation of mRNA transcription of T-cell lineage specific transcription factors was unaffected by vildagliptin treatment.
CONCLUSIONS: These data show that a four-week treatment with vildagliptin in patients with type 2 diabetes mellitus does not result in a significant modulation of cytokine responses. This observation suggests that inhibition of DDP-4 does not lead to an increased risk of infection by diminishing cytokine production.
Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

Entities:  

Keywords:  DPP-4 inhibitor; Immune function; Side effects; Type 2 diabetes

Mesh:

Substances:

Year:  2014        PMID: 24485397     DOI: 10.1016/j.diabres.2013.12.039

Source DB:  PubMed          Journal:  Diabetes Res Clin Pract        ISSN: 0168-8227            Impact factor:   5.602


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