Dermal neurovascular dysfunction in type 2 diabetes

Citation
Ai. Vinik et al., Dermal neurovascular dysfunction in type 2 diabetes, DIABET CARE, 24(8), 2001, pp. 1468-1475
Citations number
87
Categorie Soggetti
Endocrynology, Metabolism & Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
DIABETES CARE
ISSN journal
01495992 → ACNP
Volume
24
Issue
8
Year of publication
2001
Pages
1468 - 1475
Database
ISI
SICI code
0149-5992(200108)24:8<1468:DNDIT2>2.0.ZU;2-K
Abstract
OBJECTIVE - To review evidence fora relationship between dermal neurovascul ar dysfunction and other components of the metabolic syndrome of type 2 dia betes, RESEARCH DESIGN AND METHODS - We review and present data supporting concept s relating dermal neurovascular function to prediabetes and the metabolic s yndrome. Skin blood flow can be easily measured by laser Doppler techniques . RESULTS - Heat and gravity have been shown to have specific neural, nitrerg ic, and independent mediators to regulate skin blood Row. We describe data showing that this new tool identifies dermal neurovascular dysfunction in t he majority of type 2 diabetic patients, The defect in skin vasodilation is detectable before the development of diabetes and is partially correctable with insulin sensitizers. This defect is associated With C-fiber dysfuncti on (i.e., the dermal neurovascular unit) and coexists with variables of the insulin resistance syndrome. The defect most likely results from an imbala nce among the endogenous vasodilator compound nitric oxide, the vasodilator neuropeptides substance P and calcitonin gene-related peptide, and the vas oconstrictors angiotensin 11 and endothelin. Hypertension per se increases skin vasodilation and does not impair the responses to gravity, which is Op posite to that of diabetes, suggesting that the effects of diabetes overrid e and counteract those of hypertension. CONCLUSIONS - These observations suggest that dermal neurovascular function is largely regulated by peripheral C-fiber neurons and that dysregulation may be a component of the metabolic syndrome associated with type 2 diabete s.