Acute Effects of Linagliptin on Progenitor Cells, Monocyte Phenotypes, and Soluble Mediators in Type 2 Diabetes

J Clin Endocrinol Metab. 2016 Feb;101(2):748-56. doi: 10.1210/jc.2015-3716. Epub 2015 Dec 22.

Abstract

Context: Circulating cells, including endothelial progenitor cells (EPCs) and monocyte subtypes, are involved in diabetic complications. Modulation of these cells may mediate additional benefits of glucose-lowering medications.

Objective: We assessed whether the dipeptidyl peptidase-4 (DPP-4) inhibitor linagliptin acutely modifies EPCs and monocyte subsets in patients with type 2 diabetes.

Design: This was a randomized, crossover, placebo-controlled trial.

Setting: The study was conducted at a tertiary referral diabetes outpatient clinic.

Patients: Forty-six type 2 diabetes patients with (n = 18) or without (n = 28) chronic kidney disease (CKD) participated in the study.

Intervention: Intervention included a 4-day treatment with linagliptin 5 mg or placebo during two arms separated by a 2-week washout.

Main outcome measures: Before and after each treatment, we determined the levels of circulating progenitor cells (CD34, CD133, KDR) and monocyte subtypes (CD14/CD16, chemokine and scavenger receptors) and the concentrations of soluble mediators.

Results: Compared with placebo, linagliptin increased CD34(+)CD133(+) progenitor cells (placebo subtracted effect 40.4 ± 18.7/10(6); P = .036), CD34(+)KDR(+) EPCs (placebo subtracted effect 22.1 ± 10.2/10(6); P = .036), and CX3CR1(bright) monocytes (placebo subtracted effect 1.7 ± 0.8%; P = .032). Linagliptin abated DPP-4 activity by greater than 50%, significantly increased active glucagon-like peptide-1 and stromal cell-derived factor-1α, and reduced monocyte chemotactic protein-1, CCL22, and IL-12. Patients with CKD, as compared with those without, had lower baseline CD133(+) and CD34(+)CD133(+) cells and had borderline reduced CD34(+) and CD34(+)KDR(+) cells. The effects of linagliptin on progenitor cells and monocyte subtypes were similar in patients with or without CKD. Fasting plasma glucose, triglycerides and free fatty acids were unaffected.

Conclusions: DPP-4 inhibition with linagliptin acutely increases putative vasculoregenerative and antiinflammatory cells. Direct effects of DPP-4 inhibition may be important to lower vascular risk in diabetes, especially in the presence of CKD.

Trial registration: ClinicalTrials.gov NCT01617824.

Publication types

  • Randomized Controlled Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Cross-Over Studies
  • Diabetes Mellitus, Type 2 / drug therapy*
  • Dipeptidyl Peptidase 4 / metabolism
  • Dipeptidyl-Peptidase IV Inhibitors / therapeutic use
  • Endothelial Cells / drug effects
  • Female
  • Humans
  • Hypoglycemic Agents / therapeutic use*
  • Linagliptin / therapeutic use*
  • Male
  • Middle Aged
  • Monocytes / drug effects*
  • Phenotype
  • Renal Insufficiency, Chronic / complications
  • Renal Insufficiency, Chronic / metabolism
  • Stem Cells / drug effects*

Substances

  • Dipeptidyl-Peptidase IV Inhibitors
  • Hypoglycemic Agents
  • Linagliptin
  • Dipeptidyl Peptidase 4

Associated data

  • ClinicalTrials.gov/NCT01617824