Protective Effects of Niacin (Vitamin B3) on Pancreatic Functions, Hyperglycemia, Inflammatory Markers and Oxidative Stress in Alloxan-Induced Diabetic Rats | ||||
| Egyptian Journal of Veterinary Sciences | ||||
| Articles in Press, Corrected Proof, Available Online from 10 July 2025 PDF (1.67 MB) | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/ejvs.2025.379852.2814 | ||||
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| Authors | ||||
Mona Hafez1; Neveen Ragab Ashoura   2; Asmaa Ali Aboushouk3; Aya Rohiem4
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| 1Department of Physiology, Faculty Veterinary Science, Alexanddria University | ||||
| 2Department of Pharmacology, Faculty of Veterinary Medicine, Alexandria University, Alexandria, Egypt. | ||||
| 3Department of Pathology, Faculty of Veterinary Medicine, Alexandria University, Alexandria, Egypt. | ||||
| 4Department of Physiology, Faculty of Veterinary Medicine, Alexandria University, Alexandria, Egypt. | ||||
| Abstract | ||||
| Numerous studies and experiments have revealed that the initiation and progression of type 2 diabetes mellitus is majorly triggered by oxidative stress. Niacin, generally referred to as vitamin B3, is a critical vitamin that is considered a significant food additive as it eliminates free radical damage. This investigation aimed to test the extent to which a diabetic environment is affected by antioxidants with nutraceutical potential. Four distinct experimental treatment groups were established for the 32 albino rats after the intraperitoneal infusion of Alloxan (120 mg/kg Bwt) to induce diabetes. These groups include the standard control, niacin (15 mg/kg Bwt), diabetic control, and diabetic niacin-treated groups. Blood and pancreatic tissue samples were collected from animals euthanized after four weeks to evaluate various biochemical and histological alterations. The expressions of insulin in β cell islets were also assessed using immunohistochemistry analysis. In diabetic rats, several physiological changes were observed, including Increased values of hyperglycemia, tumour necrosis factor-α (TNF-α), pancreatic malondialdehyde and interleukin-1β and 6 (IL-1β and IL-6). Additionally, there were decreased levels of plasma insulin and pancreatic antioxidants, specifically reduced concentrations of superoxide dismutase (SOD), reduced glutathione (GSH), and catalase (CAT). Furthermore, limited positive insulin immunoreactivity was linked to histological alterations in the pancreatic islets in the diabetic group compared to the standard control one. The activities and structure of β cells were significantly restored and recovered after niacin therapy. There was a discernible drop in oxidative stress markers as fasting blood glucose levels decreased. Dietary niacin supplementation could relieve diabetes mellitus symptoms owing to its hypoglycemic, antioxidant, and anti-inflammatory properties. | ||||
| Keywords | ||||
| β Cell function; Diabetes mellitus; Inflammation; Oxidative stress; Pancreas | ||||
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