Genetic and epigenetic factors contribute equally to the pathogenesis of type 1 diabetes mellitus. Sodium butyrate (NaB) has been reported to improve glucose homeostasis by modulation of the p38/ERK MAPK pathway. This work aims to evaluate the effect of NaB on the ultrastructure of pancreatic β-cells and the PI3/AKT pathway. Juvenile albino male rats were used to establish a type 1 diabetes model using streptozotocin injection and NaB in a pre- and post-treatment schedule. Plasma glucose, insulin levels, and glucose tolerance were evaluated. Light and electron microscopy and immunohistochemistry were performed using Ki-67, caspase-3, and insulin. NaB treatment resulted in a significant improvement in plasma glucose levels, plasma insulin levels/expression, and ameliorated diabetes-induced histological alternations. Additionally, it increased the expression of phosphorylated AKT. These findings provide evidence that NaB may be useful in the treatment of juvenile diabetes.

中文翻译：

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胰腺β细胞的超微结构表征伴随着HDAC抑制剂丁酸钠对幼年糖尿病大鼠PI3 / AKT胰岛素信号通路的调节作用。

遗传因素和表观遗传因素对1型糖尿病的发病机理具有同等的作用。据报道，丁酸钠（NaB）可通过调节p38 / ERK MAPK途径来改善葡萄糖稳态。这项工作旨在评估NaB对胰腺β细胞超微结构和PI3 / AKT途径的影响。在治疗前后，使用链脲佐菌素注射液和NaB，将幼年的白化病雄性大鼠用于建立1型糖尿病模型。评估血浆葡萄糖，胰岛素水平和葡萄糖耐量。使用Ki-67，caspase-3和胰岛素进行光镜和电子显微镜及免疫组化。NaB治疗可显着改善血浆葡萄糖水平，血浆胰岛素水平/表达，并改善糖尿病引起的组织学改变。此外，它增加了磷酸化AKT的表达。这些发现提供了NaB可能在青少年糖尿病治疗中有用的证据。