Erythropoietin, Myoinositol and Metformin modulate Insulin Sensitivity Indices, Pancreatic Beta Cell Mass and hepatocellular changes in a Rat Model of PCO | ||||
Ain Shams Medical Journal | ||||
Articles in Press, Accepted Manuscript, Available Online from 01 October 2024 | ||||
Document Type: Original Article | ||||
DOI: 10.21608/asmj.2022.178067.1075 | ||||
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Authors | ||||
sherine ahmed mohammed ![]() ![]() | ||||
1department of histology, faculty of medicine, sohag university | ||||
2department of physiology, faculty of medicine, sohag university. | ||||
3department of physiology , faculty of medicine, sohag university | ||||
4department of physiology, faculty of medicine, sohag university | ||||
Abstract | ||||
Abstract: Background: Polycystic ovary (PCO) is a common health problem in females throughout their reproductive age. Common symptoms of PCO are hyperandrogenemia, infertility, and menstrual disorders. Metabolic disorders like insulin resistance and steatotic liver are also common. Objective: This study aimed to compare the potential therapeutic role of erythropoietin, myoinositol, and the widely used metformin drug against hyperinsulinemia and hepatic injury of letrozole-induced PCOS model in rats. Materials and methods: fifty female Wistar rats were classified equally into five groups: The control group, PCO model group: PCO model was induced by letrozole in a dose of 0.5 mg/kg daily for 3 weeks. Then rats with PCO were administrated for the following 21 days: erythropoietin (EPO/PCO) group, myoinositol (MYO/PCO) group, or metformin (MET/PCO) group. Biochemical and histological studies on the liver and pancreas were done. Immunohistochemical staining with GLUT-1 and insulin was done. Results: PCOS rats developed insulin resistance with pancreatic β cell degeneration, hepatocellular injury and upregulation of hepatic GLUT-1. Conclusion: erythropoietin was most effective in restoring B cell mass, decreasing hyperinsulinemia associated with letrozole -induced PCOS model, and attenuating hepatocellular degeneration via reduction of stress induced hepatic GLUT-1. | ||||
Keywords | ||||
polycystic ovary; hyperinsulinmia; GLUT-1; pancreas | ||||
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