Effect of Butyrate Extracted From Clostridium Butyricum Bacteria on Insulin Receptor Phosphorylation in Liver and Muscle Cells in Mice

Butyrate extracted from C. butyricum acts as a potent metabolic modifier that repairs defects in the insulin signaling pathway. This compound contributes to reducing insulin resistance through dual mechanisms, making it a promising biopharmaceutical candidate for therapeutic enhancement in patients with diabetes and obesity. The role of a short chain fatty acid (SCFA) generated through the fermentation of Clostridium butyricum bacteria was examined to determine its role in improving insulin sensitivity. The main aim of this study was to determine the efficiency of insulin receptor (IR) phosphorylation in the liver and muscle of mice models of in vitro-induced diabetes. The research employed advanced selective and extractive fermentation techniques to produce highly purified butyrate (91%). Mice were divided into experimental groups, including a control group and groups treated with butyrate and magnesium. Using Western blotting to estimate the ratio of active phosphorylation (p-IR) to total protein (Total-IR), and using immunohistochemically assay (IHC) to track glucose transporter expression. In the liver, the treatment resulted in activation of AMPK protein and a reduction in oxidative stress and triglyceride accumulation, leading to inhibition of gluconeogenesis. At the genetic level, butyrate acted as an inhibitor of HDAC enzymes, improving the expression of genes associated with insulin sensitivity.