Abstract
Xeroderma is a frequent complication in diabetic patients. In this study, we investigated the mechanism underlying the onset of diabetic xeroderma, focusing on aquaporin-3 (AQP3), which plays an important role in water transport in the skin. Dermal water content in diabetic mice was significantly lower than that in control mice. The expression level of AQP3 in the skin was significantly lower in diabetic mice than in control mice. One week after streptozotocin (STZ) treatment, despite their increased blood glucose levels, mice showed no changes in the expression levels of AQP3, Bmal1, Clock, and D site-binding protein (Dbp) in the skin and 8-hydroxydeoxyguanosine (8-OHdG) in the urine. In contrast, two weeks after STZ treatment, mice showed increases in the blood glucose level, decreases in AQP3, Bmal1, Clock, and Dbp levels, and increases in the urinary levels of 8-OHdG. The results of this study suggest that skin AQP3 expression decreases in diabetes, which may limit water transport from the vessel side to the corneum side, causing dry skin. In addition, in diabetic mice, increased oxidative stress triggered decreases in the expression levels of Bmal1 and Clock in the skin, thereby inhibiting the transcription of Aqp3 by Dbp, which resulted in decreased AQP3 expression.
Highlights
The number of diabetic patients continues to increase with changes in lifestyle and social environments [1]
We examined whether the water channel AQP3 expressed in the skin is involved in the onset this study, we examined whether the water channel AQP3 expressed in the skin is involved in the mechanism of diabetic xeroderma
Analysis of the expression levels of skin AQP3 in mice at four weeks after STZ treatment revealed significant decreases at both the mRNA and protein levels compared with the levels in control revealed significant decreases at both the mRNA and protein levels compared with the levels in group mice
Summary
The number of diabetic patients continues to increase with changes in lifestyle and social environments [1]. Subjective symptoms such as polyuria and thirst occur as initial symptoms, and nephropathy, retinopathy, and peripheral neuropathy develop as the disease progresses further. In addition to these complications, many patients develop various skin diseases, and the proportion of these patients is approximately 80% in clinical practice [2,3,4]. Xeroderma is characterized by dryness of the skin due to loss of moisture and occurs in 1 out of 4 diabetic patients. The prevention and treatment of xeroderma are important because this condition reduces patient quality of life but can cause other skin diseases, such as skin infections and gangrene. Elucidation of the mechanism underlying the onset of diabetic xeroderma has been attempted for the purposes of prevention and treatment [5], but this mechanism is not yet fully understood
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