Greater circulating DPP4 activity is associated with impaired flow-mediated dilatation in adults with type 2 diabetes mellitus.


Journal

Nutrition, metabolism, and cardiovascular diseases : NMCD
ISSN: 1590-3729
Titre abrégé: Nutr Metab Cardiovasc Dis
Pays: Netherlands
ID NLM: 9111474

Informations de publication

Date de publication:
10 2019
Historique:
received: 27 02 2019
revised: 01 07 2019
accepted: 15 07 2019
pubmed: 23 8 2019
medline: 20 2 2020
entrez: 22 8 2019
Statut: ppublish

Résumé

Dipeptidyl peptidase 4 (DPP4) is a key enzyme involved in the regulation of the incretin system exerted by cleaving the glucagon-like peptide 1 (GLP-1); the blockage of DPP4, exerted by the antidiabetic agents DPP4-inhibitors (DPP4-I), results in greater GLP-1 concentration and improved glycaemic control. DPP4 acts also as a pro-inflammatory molecule and mediates vascular damage in experimental models. The relationship between DPP4 activity and endothelial function in diabetes has not been explored yet. Aim of this study was to investigate systemic plasma DPP4 activity in relation to endothelial function in patients with type 2 diabetes mellitus (T2DM). Sixty-two T2DM individuals were recruited in our Diabetes outpatient clinics, Sapienza University, Rome, Italy. All participants underwent complete clinical work-up; endothelial function was evaluated by flow-mediated dilatation (FMD) test; plasma DPP4 activity was assessed by measuring the 7-amino-4-methylcoumarin (AMC) cleavage rate from the synthetic substrate H-glycyl-prolyl-AMC and compared with DPP4 activity measured in sixty-two age-, sex-, BMI-matched non-diabetic subjects. Patients with T2DM had significantly higher DPP4 activity than non-diabetic individuals (211,466 ± 87657 vs 158,087 ± 60267 nmol/min/ml, p < 0.001); in T2DM patients, greater DPP4 activity significantly correlated with lower FMD whereas was not associated with BMI and metabolic control. Greater systemic DPP4 activity was an independent predictor of reduced FMD after adjusting for age, gender and other confounders. Circulating DPP4 activity is increased in individuals with T2DM and associated with signs of endothelial dysfunction such as impaired FMD. DPP4 may negatively affect endothelial function through mechanisms beyond glucose homeostasis and metabolic control.

Sections du résumé

BACKGROUND AND AIM
Dipeptidyl peptidase 4 (DPP4) is a key enzyme involved in the regulation of the incretin system exerted by cleaving the glucagon-like peptide 1 (GLP-1); the blockage of DPP4, exerted by the antidiabetic agents DPP4-inhibitors (DPP4-I), results in greater GLP-1 concentration and improved glycaemic control. DPP4 acts also as a pro-inflammatory molecule and mediates vascular damage in experimental models. The relationship between DPP4 activity and endothelial function in diabetes has not been explored yet. Aim of this study was to investigate systemic plasma DPP4 activity in relation to endothelial function in patients with type 2 diabetes mellitus (T2DM).
METHODS AND RESULTS
Sixty-two T2DM individuals were recruited in our Diabetes outpatient clinics, Sapienza University, Rome, Italy. All participants underwent complete clinical work-up; endothelial function was evaluated by flow-mediated dilatation (FMD) test; plasma DPP4 activity was assessed by measuring the 7-amino-4-methylcoumarin (AMC) cleavage rate from the synthetic substrate H-glycyl-prolyl-AMC and compared with DPP4 activity measured in sixty-two age-, sex-, BMI-matched non-diabetic subjects. Patients with T2DM had significantly higher DPP4 activity than non-diabetic individuals (211,466 ± 87657 vs 158,087 ± 60267 nmol/min/ml, p < 0.001); in T2DM patients, greater DPP4 activity significantly correlated with lower FMD whereas was not associated with BMI and metabolic control. Greater systemic DPP4 activity was an independent predictor of reduced FMD after adjusting for age, gender and other confounders.
CONCLUSIONS
Circulating DPP4 activity is increased in individuals with T2DM and associated with signs of endothelial dysfunction such as impaired FMD. DPP4 may negatively affect endothelial function through mechanisms beyond glucose homeostasis and metabolic control.

Identifiants

pubmed: 31431395
pii: S0939-4753(19)30278-9
doi: 10.1016/j.numecd.2019.07.010
pii:
doi:

Substances chimiques

Biomarkers 0
DPP4 protein, human EC 3.4.14.5
Dipeptidyl Peptidase 4 EC 3.4.14.5

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1087-1094

Informations de copyright

Copyright © 2019 The Italian Society of Diabetology, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition, and the Department of Clinical Medicine and Surgery, Federico II University. All rights reserved.

Auteurs

Ilaria Barchetta (I)

Department of Experimental Medicine, Sapienza University of Rome, Italy.

Gea Ciccarelli (G)

Department of Experimental Medicine, Sapienza University of Rome, Italy.

Eugenio Barone (E)

Department of Biochemical Sciences, Sapienza University of Rome, Italy.

Flavia A Cimini (FA)

Department of Experimental Medicine, Sapienza University of Rome, Italy.

Valentina Ceccarelli (V)

Department of Experimental Medicine, Sapienza University of Rome, Italy.

Laura Bertoccini (L)

Department of Experimental Medicine, Sapienza University of Rome, Italy.

Federica Sentinelli (F)

Department of Experimental Medicine, Sapienza University of Rome, Italy.

Antonella Tramutola (A)

Department of Biochemical Sciences, Sapienza University of Rome, Italy.

Maria Del Ben (M)

Department of Internal Medicine and Medical Specialties, Sapienza University of Rome, Italy.

Francesco Angelico (F)

Department of Internal Medicine and Medical Specialties, Sapienza University of Rome, Italy.

Marco G Baroni (MG)

Department of Experimental Medicine, Sapienza University of Rome, Italy.

Andrea Lenzi (A)

Department of Experimental Medicine, Sapienza University of Rome, Italy.

Maria G Cavallo (MG)

Department of Experimental Medicine, Sapienza University of Rome, Italy. Electronic address: gisella.cavallo@uniroma1.it.

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Classifications MeSH