Naringin Ameliorates Streptozotocin-Induced Diabetes through Forkhead Box M1-Mediated Beta Cell Proliferation

Adult pancreatic beta cells, though quiescent, can proliferate in response to physiological need. This inherent character is used in exploring the possibilities of expanding the beta cell mass in the treatment of diabetes. Forkhead box M1 (FoxM1) transcription factor is an important regulator in the proliferation and survival of adult beta cell mass. Naringin, a flavanone glycoside, is reported to have antidiabetic activity and exhibited an increase in insulin levels in diabetic animals.

The present study tried to evaluate the role of naringin in the regulation of FoxM1 in the pancreas of diabetic rats and to reascertain its antilipidemic and antioxidant properties.

Diabetes was induced in male rats using streptozotocin and treated with naringin (100 mg/kg) orally for 4 and 8 weeks. Serum biochemical parameters, insulin, gene and protein expression of FoxM1, and antioxidant markers in rat pancreas were analyzed.

Naringin administration reduced the blood sugar, urea, creatinine, and cholesterol values and improved the pancreatic antioxidant status in diabetic rats. Naringin-treated diabetic rats showed a significant increase in mRNA and protein expression of FoxM1 compared to the diabetic control rats, indicating regeneration of cells. It also increased the insulin immunopositive cells, indicating functional beta cells.

Naringin was found to upregulate the FoxM1 transcription factor in diabetic animals, which influenced the proliferation and functional status of beta cells.