Department of Pharmaceutical Sciences, Suzuka University of Medical Science, Suzuka, Japan.
Research Laboratories, Nichinichi Pharmaceutical Co., Ltd., Iga, Japan.
Int J Med Sci. 2021 Jan 1;18(2):474-481. doi: 10.7150/ijms.50764. eCollection 2021.
Diabetes induces dry skin that may cause infective diseases. In this study, we aimed to clarify the mechanism of diabetes-induced skin dryness in animal models. We also examined the difference in the mechanism of skin dryness in type 1 and type 2 diabetes. We examined skin dryness in type 1 diabetes model mice (streptozotocin [STZ] induction), non-obesity type 2 diabetes model mice (newborn STZ injection), and obesity type 2 diabetes model mice (KK-Ay/TaJcl). An increase in transepidermal water loss was observed in the type 1 diabetes model mice, and reduced skin hydration was observed in the type 2 diabetes model mice. In the type 1 diabetes model mice, an increase in advanced glycation end products and matrix metalloproteinase-9 led to a decline in collagen IV level, inducing skin dryness. In the obesity type 2 diabetes model mice, an increase in the release of histamine and hyaluronidase by mast cells resulted in a decline in the level of hyaluronic acid, inducing skin dryness. However, in the non-obesity type 2 diabetes model mice, the main factors of skin dryness could not be clearly identified. Nevertheless, inflammatory cytokine levels increased. We hypothesize that inflammatory cytokines disrupt the collagen of the skin. Diabetes caused skin dryness in each mouse model, and the mechanism of skin dryness differed by diabetes type.
糖尿病会导致皮肤干燥,从而可能引发感染性疾病。在本研究中,我们旨在阐明动物模型中糖尿病引起皮肤干燥的机制。我们还研究了 1 型和 2 型糖尿病皮肤干燥机制的差异。我们检查了 1 型糖尿病模型小鼠(链脲佐菌素[STZ]诱导)、非肥胖型 2 型糖尿病模型小鼠(新生 STZ 注射)和肥胖型 2 型糖尿病模型小鼠(KK-Ay/TaJcl)的皮肤干燥情况。在 1 型糖尿病模型小鼠中观察到经皮水分丢失增加,在 2 型糖尿病模型小鼠中观察到皮肤水合作用降低。在 1 型糖尿病模型小鼠中,晚期糖基化终产物和基质金属蛋白酶-9 的增加导致胶原 IV 水平下降,从而导致皮肤干燥。在肥胖型 2 型糖尿病模型小鼠中,肥大细胞释放的组胺和透明质酸酶增加导致透明质酸水平下降,从而导致皮肤干燥。然而,在非肥胖型 2 型糖尿病模型小鼠中,皮肤干燥的主要因素尚不清楚。尽管如此,炎症细胞因子水平增加。我们假设炎症细胞因子破坏了皮肤的胶原蛋白。糖尿病导致每个小鼠模型的皮肤干燥,并且皮肤干燥的机制因糖尿病类型而异。