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Experimental Diabetes Research
Volume 2012, Article ID 892706, 11 pages
Clinical Study

Dipeptidyl Peptidase 4 Inhibition May Facilitate Healing of Chronic Foot Ulcers in Patients with Type 2 Diabetes

1Department of Geriatrics and Metabolic Diseases, Second University of Naples, 80138 Naples, Italy
2Department of Internal and Experimental Medicine, Center of Cardiovascular Excellence, Second University of Naples, 80138 Naples, Italy
3Department of Geriatric Surgery, Second University of Naples, 80138 Naples, Italy
4Department of Biochemistry, Section of Pathology, Second University Naples, 80138 Naples, Italy
5Department of Pharmaceutical Sciences, University of Salerno, Salerno 84084, Italy

Received 1 June 2012; Revised 12 September 2012; Accepted 12 September 2012

Academic Editor: N. Cameron

Copyright © 2012 Raffaele Marfella et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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-1α 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.