Department of Medicine, University College London, London, United Kingdom, School of Biological and Chemical Sciences, Birkbeck University of London, United Kingdom
The generation of thickened plantar stratum corneum (SC) in response to elevated pressures, places individuals with diabetes at risk of ulceration. Such a response may culminate from altered biochemical and physical states of the epidermis as a result of non-enzymatic glycation (NEG). The objective of this study was to quantify specific glycation products generated in plantar epidermal proteins in individuals with Type 2 Diabetes Mellitus (T2DM) and age-matched controls (n = 103 and n = 87, respectively) and to compare these data with the viscoelastic properties (in vivo) of the epidermis. Plantar SC and venous blood samples were collected from all participants for the quantification of furosine and pentosidine using high performance liquid chromatography (HPLC). The viscoelastic properties of plantar epidermis were measured by the application of negative pressure on the surface of the skin. Plantar epidermal thickness was measured using high frequency (20 MHz) ultrasonography. There was a significantly greater concentration of pentosidine in the SC samples from people with T2DM (p = 0.001). There was no correlation between the concentration of glycated proteins in the epidermal proteins and serum proteins (furosine r = – 0.115, pentosidine r = – 0.023). The plasticity of the epidermis was significantly lower in the T2DM group than the control group (p = 0.007). The results suggest that alterations in the glycation of plantar epidermal proteins may constitute additional aggravators of ulceration in people with T2DM.