z-logo
open-access-imgOpen Access
Dipeptidyl Peptidase 4 Inhibition May Facilitate Healing of Chronic Foot Ulcers in Patients with Type 2 Diabetes
Author(s) -
Raffaele Marfella,
Ferdinando Carlo Sasso,
Maria Rosaria Rizzo,
Pasquale Paolisso,
Michelangela Barbieri,
Vincenzo Padovano,
Ornella Carbonara,
Pasquale Gualdiero,
Pasquale Petronella,
Franca Ferraraccio,
Antonello Petrella,
Raffaele Caico,
Ferdinando Campitiello,
Angela Della Corte,
Giuseppe Paolisso,
Silvestro Caico
Publication year - 2012
Publication title -
experimental diabetes research
Language(s) - English
Resource type - Journals
eISSN - 1687-5303
pISSN - 1687-5214
DOI - 10.1155/2012/892706
Subject(s) - medicine , pathophysiology , dipeptidyl peptidase 4 , incretin , angiogenesis , vildagliptin , wound healing , diabetic foot , diabetes mellitus , pathological , complication , type 2 diabetes , dipeptidyl peptidase , bioinformatics , surgery , endocrinology , enzyme , biochemistry , chemistry , biology
The pathophysiology of chronic diabetic ulcers is complex and still incompletely understood, both micro- and macroangiopathy strongly contribute to the development and delayed healing of diabetic wounds, through an impaired tissue feeding and response to ischemia. With adequate treatment, some ulcers may last only weeks; however, many ulcers are difficult to treat and may last months, in certain cases years; 19–35% of ulcers are reported as nonhealing. As no efficient therapy is available, it is a high priority to develop new strategies for treatment of this devastating complication. Because experimental and pathological studies suggest that incretin hormone glucagon-like peptide-1 may improves VEGF generation and promote the upregulation of HIF-1 α through a reduction of oxidative stress, the study evaluated the effect of the augmentation of GLP-1, by inhibitors of the dipeptidyl peptidase-4, such as vildagliptin, on angiogenesis process and wound healing in diabetic chronic ulcers. Although elucidation of the pathophysiologic importance of these aspects awaits further confirmations, the present study evidences an additional aspect of how DPP-4 inhibition might contribute to improved ulcer outcome.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here
Accelerating Research

Address

John Eccles House
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom