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.
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