Animal models and experimental medicine · 2025
Adropin modulates pancreatic cell proliferation and glutathione levels in an animal model of type 1 diabetes mellitus.
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Ali Ifrah I, D'Souza Crystal, Nemmar Abderrahim, Ojha Shreesh, Adeghate Ernest A
Аннотация
BACKGROUND: Diabetes mellitus (DM), a metabolic disorder that leads to chronic hyperglycemia, is one of the topmost global public health concerns according to the International Diabetes Federation. Adropin is a peptide hormone that is primarily involved in energy homeostasis, but its involvement in other biological activities such as lowering hyperlipidemia, and diminishing insulin resistance has also been reported. In this study, we aimed to explore additional effects of adropin on oxidative stress, inflammation, and cell proliferation in an animal model of type 1 DM.
METHODS: To achieve our aim, normal and diabetic Wistar rats were treated with adropin (2.1 μg/kg/day) for a period of 10 days. Pancreatic tissue samples were collected for histomorphological analysis and inflammation assay, while blood was collected for oxidative stress assay.
RESULTS: Our results showed that diabetes induction stimulated cell proliferation in both exocrine and endocrine pancreas, and adropin dramatically attenuated this effect in pancreatic exocrine tissue, but not in the islet of Langerhans. In addition, adropin significantly increased glutathione reductase expression in pancreatic tissue, and augmented serum total glutathione in the diabetic rats compared to diabetic untreated rats.
CONCLUSION: Our study indicates the potential role of adropin in alleviating oxidative stress in DM.
METHODS: To achieve our aim, normal and diabetic Wistar rats were treated with adropin (2.1 μg/kg/day) for a period of 10 days. Pancreatic tissue samples were collected for histomorphological analysis and inflammation assay, while blood was collected for oxidative stress assay.
RESULTS: Our results showed that diabetes induction stimulated cell proliferation in both exocrine and endocrine pancreas, and adropin dramatically attenuated this effect in pancreatic exocrine tissue, but not in the islet of Langerhans. In addition, adropin significantly increased glutathione reductase expression in pancreatic tissue, and augmented serum total glutathione in the diabetic rats compared to diabetic untreated rats.
CONCLUSION: Our study indicates the potential role of adropin in alleviating oxidative stress in DM.