| Summary: | Diabetes mellitus, one of the major metabolic threats to human health has elevated drastically all along the twenty-first century. Insulin that is released by beta-cells of the pancreas is the primary hormone linked to diabetes, and it directs the flow of glucose into muscle and blood. The insulin receptor helps in binding up glycogen synchronized hormone that is insulin which has two extracellular α and two transmembrane β subunits. The intracellular subunit or domain known as the tyrosine kinase domain activates once the insulin gets bound to the extracellular subunit followed by the activation of the insulin receptor substrate family (IRSI-4) which stimulates the PI3K/Akt pathway that is a key signaling system that controls apoptosis, cell proliferation, and a variety of other cell activities. The regulatory governmental subunit PIK3R1 heterodimer binds with the tyrosin-phosphorylated form via SH2 domains, allowing PIK3R1 to be recruited to the specified receptor, promoting PI3K activity. β- glucan plays a significant role in regulating the PI3K/Akt biochemical pathway via IRS1, PI3K-p85, and phosphorylated Akt, which increases insulin sensitivity and reduces the associated risks. Additionally, administration of these polysaccharides boosts GLUT4 concentrations in the pancreas and depresses glycogen synthase kinase-3 β levels across most cells, indicating that β-glucan serves as an anti-diabetic drug by activating the PI3K/Akt/GSK-3/GLUT-4 signal transduction pathways. Hence, the purpose of this review is to shed light on the activity and mechanism of the PIK3R1 gene on naturally produced β-glucan in the etiology of diabetes.
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