AI Article Synopsis

  • PDX-1 is a crucial transcription factor involved in insulin gene regulation and maintaining β-cell mass, while naringin is a flavanone known for its antioxidant and potential antidiabetic properties.
  • The study involved inducing diabetes in rats and treating them with naringin for 4 and 8 weeks, focusing on changes in serum insulin, PDX-1 expression, and pancreatic health.
  • Results showed that naringin treatment improved β-cell function and increased PDX-1 and insulin gene expression, with the most significant effects observed after 8 weeks, indicating naringin's effectiveness as an antidiabetic agent.

Article Abstract

Background: Pancreatic duodenal homeobox-1 (PDX-1) is a key transcription factor which regulates Insulin gene expression and insulin secretion in adult β-cells and helps to maintain β-cells mass. Naringin, a flavanone, owing to its anti-oxidant property, is reported to have antidiabetic effects.

Objectives: The present study tries to evaluate the role of naringin on the β-cell-specific transcription factor PDX-1 in diabetic rats.

Methods: Diabetes was induced in male rats using streptozotocin and treated with naringin (100 mg/kg) orally for 4 and 8 weeks. Serum insulin level, Pdx-1 and Insulin gene expression, and PDX-1 protein expression were assessed in the rat pancreas. Histopathological and ultrastructural changes in the islet and β-cells were observed.

Results: Naringin prevented leukocytic infiltration in the pancreas of diabetic rats and recouped the β-cells with adequate secretory granules. Naringin-treated diabetic rats showed significantly increased mRNA expression of Pdx-1 and Insulin genes, increased expression of transcription factor PDX-1, and higher serum insulin levels than the diabetic control animals. These changes were more pronounced in the 8-week naringin-treated diabetic animals.

Conclusions: Naringin was found to be an effective antidiabetic agent which increased Insulin gene expression and insulin secretion by upregulating the PDX-1 gene and protein expression.

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Source
http://dx.doi.org/10.1159/000496506DOI Listing

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