Extracellular matrix macromolecules such as collagen and fibronectin are progressively altered during aging and diabetes. A number of pathways are activated in the hyperglycemic milieu and in diabets, such as the aldose reductase pathway (AR), activation of protein kinase C (PKC), especially the β isoform, and the generation of advanced glycation end products (AGE). Activation of these pathways has been demonstrated in glucose-treated glomeruli or mesangial cells.

In the present study, we explored the effect of high glucose levels, mimicking diabetic conditions, on the expression of type I and III collagen, the most abundant matrix protein, in cultured human skin fibroblasts. Total RNA was extracted from human dermal fibroblasts incubated with varying amounts of glucose: 1 g/l (normoglycemic), 2, 4 and 6 g/l (hyperglycemic) D-glucose for 24 hours and mRNA expression of type I and III collagen was analyzed by quantitative real-time PCR.

Incubation of human dermal fibroblasts with high glucose concentration resulted in a significant increase of procollagen-α1 (I) mRNA collagen type I expression in a dose-dependent manner whereas expression of collagen III was unaffected.

Our results suggest that high level of glucose may influence the process of skin aging through mild stimulation of collagen type I synthesis and possible of other extracellular matrix proteins. The change in the ratio of collagen I /collagen III expression and the increase of the synthesis of collagen contributes to a decreased tensile strength and mechanical stability of both the connective tissues and the induced scar tissue in patience with diabetes.