Abstract
PURPOSE: The purpose of the study was to determine how camel milk affects hyperglycemia, beta-cell function, oxidative stress, and inflammatory markers in type 2 diabetic pigs. METHODS: Twenty-five (25) pigs were separated into five (5) groups of five pigs each, with five (5) non-diabetic and twenty (20) diabetic pigs in each group. Groups 1 and 2 received distilled water as the standard control and diabetic control groups, respectively, while Groups 3 and 4 received camel milk at 250 mL/day and 500 mL/day, respectively, and Group 5 received metformin at 500 mg/day. The experiment lasted ten weeks. At the end of the ten weeks, all the pigs were euthanized. RESULTS: Treatments with camel milk substantially enhance glucose fasting levels by reducing hyperglycemia in diabetic pigs, significant level at (p < 0.05). When pigs given camel milk were compared with untreated diabetic pigs, there was a substantial rise (p < 0.05) in superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (GSH) levels. Also, camel milk substantially lowered the levels of interleukin (IL-1β) and tumour necrosis factor-alpha (TNF-α) in diabetic pig serum. Similarly, immunohistochemical analysis of islet cells revealed an increase in insulin production, implying improved glycemic control and the eventual commitment of glucose to glycolysis. CONCLUSION: The bioactive-mediated anti-hyperglycemic and insulin release potential of camel milk treatments contributed to improving type 2 diabetes mellitus. Camel milk improved beta-cell function while reducing oxidative stress and inflammation in type 2 diabetic pigs.