Role of Cutaneous Aquaporins in the Development of Xeroderma in Type 2 Diabetes

• Main Authors: Nobutomo Ikarashi, Nanaho Mizukami, Chenchen Pei, Ryogo Uchino, Izumi Fujisawa, Natsuko Fukuda, Risako Kon, Hiroyasu Sakai, Junzo Kamei
• Format: Article
• Language: English
• Published: MDPI AG 2021-01-01
• Series: Biomedicines
• Subjects: diabetes; aquaporin; skin; xeroderma; inflammation; TNF-α
• Online Access: https://www.mdpi.com/2227-9059/9/2/104

Xeroderma is induced by diabetes, reducing patients’ quality of life. We aimed to clarify the roles of cutaneous water channel aquaporin-3 (AQP3) in diabetic xeroderma using type 2 diabetes model <i>db/db</i> mice. Blood glucose levels were unchanged in 5-week-old<i> db/db</i> mice compared to <i>db/+ </i>mice (control mice), but the pathophysiology of type 2 diabetes was confirmed in 12-week-old <i>db/db</i> mice. The dermal water content and AQP3 expression in 5-week-old <i>db/db</i> mice were almost the same as those in the control mice. On the other hand, in 12-week-old <i>db/db </i>mice, the dermal water content and AQP3 expression were significantly decreased. The addition of glucose to HaCaT cells had no effect on AQP3, but tumor necrosis factor-α (TNF-α) decreased the AQP3 expression level. Blood TNF-α levels or skin inflammation markers in the 12-week-old <i>db/db</i> mice were significantly higher than those in control mice. AQP3 levels in the skin were decreased in type 2 diabetes, and this decrease in AQP3 may be one of the causes of xeroderma. Therefore, a substance that increases AQP3 may be useful for improving xeroderma. Additionally, a decrease in skin AQP3 may be triggered by inflammation. Therefore, anti-inflammatory drugs may be effective as new therapeutic agents for diabetic xerosis.