Correlates of dermis thickness in mouse models with a range of obesity, insulin resistance and diabetic states

Abstract

Diabetic complications of the skin regarding skin structure have been well documented and researched, notably in relation to wound healing. Recently it has also been discovered that dermis thickness may also be reduced in type 2 diabetic patients. Peripheral damage in diabetes has been attributed to inflammation, as well as hyperglycaemia resulting from insulin resistance. However, this has not been investigated specifically in relation to dermis thickness. This study used mouse models with a range of obesity, insulin resistance and diabetic states to investigate the extent of reduction in dermis thickness that results from these conditions and to elucidate the correlation of dermis thickness with both biomarkers of insulin resistance and whole-body and local proinflammatory cytokine levels, which can both directly damage tissues and be the causative factor of the insulin resistance. The results suggest that the reduced dermis thickness observed in type 2 diabetes is likely a result of hyperglycaemia resulting from insulin resistance rather than the increased proinflammatory milieu resulting from insulin resistance and obesity.