Background: Insulin resistance, hyperinsulinemia, and hyperglycemia are hallmarks of type 2 diabetes (T2DM). T2DM's hyperglycemia is caused by an unusually high hepatic gluconeogenesis, which results in an increase in glucose production. Gluconeogenesis inhibition is the primary mechanism by which Metformin cures hyperglycemia. Gluconeogenic gene expression has been regulated by Sirtuin 1 (SIRT1). A new method for studying how metformin affects the levels and activity of SIRT1 in the liver and kidneys of diabetic rats is described in this research.
SIRT1 will also be studied for its probable impact on diabetes-related metabolic problems, such as elevated blood glucose levels.This is a novel method of how metformin affected SIRT-1 levels and activity in diabetic rat's liver and pancreas.
Further, the possible role of SIRT-1 on metabolic disorders associated with diabetes mellitus, including serum levels of glucose tests will be explored.
Method:24 male albino rats were divided into control group (Gp I) , DM diabetic group(Gp II) were induced by alloxan 150 mg/kg ,( metformin+ DM) group (Gp III) and (nanoparticles+ DM) group (Gp IV) whereeach rat received 45 mg/kg metformin daily for 28 days after being induced with diabetes by alloxan.
At the end of study : Serum glucose levels and SIRT1gene expression in the liver and kidneys were measured at 7 and 28 days.
Results : Glucose levels were much lower for seven days and SIRT-1expression levels in the liver and kidneys were significantly upregulated according to our results.
Conclusion : Metformin nanoparticles, rather than metformin, improved diabetes patients' SIRT1 levels.