Camel milk ameliorates diabetes in pigs by preventing oxidative stress, inflammation and enhancing beta cell function

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.

Keywords: Camel milk; Hyperglycemia; Inflammatory markers; Oxidative stress; Pancreas.

Fig. 1

Body weight of the experimental, (a) Mean weights of the pigs over the experimental period (b) change in body weight bar charts. n = 5, NC = non-diabetic, D-HFD = diabetic control, CM = camel milk, MET = metformin

Fig. 2

Line graph of fasting glucose level, at every two weeks interval for the period of 10 weeks of treatment. Data were analysed using one way ANOVA, followed with Tukey post hoc test. n = 5, NC = non-diabetic, D-HFD = diabetic control, CM = camel milk, MET = metformin

Fig. 3

Bar charts of Oxidative stress parameters ((a) SOD, (b) CAT, (c) GSH and (d) MDA) after 10 weeks of treatment. Data were analysed using one way ANOVA, followed with Tukey post hoc test. n = 5, NC = non-diabetic, D-HFD = diabetic control, CM = camel milk, MET = metformin

Fig. 4

Bar charts of Inflammatory parameters (a) Serum IL-1β levels, (b) Serum TNF-α levels after 10 weeks of treatment. Data were analysed using one way ANOVA, followed with Tukey post hoc test. n = 5, NC = non-diabetic, D-HFD = diabetic control, CM = camel milk, MET = metformin

Fig. 5

Composite photomicrographs of non-diabetic and diabetic pig pancreas showing normal beta-cells (A), degranulation of beta-cells (B), and regenerating beta-cells (C, D, & E). H&E X250. A = pancreas of normal control pigs, B = pancreas of diabetic control pigs, C = pancreas of pigs treated with 250 mL/day Camel milk, D = pancreas of pigs treated with 500 mL/day Camel milk, E = pancreas of pigs treated with Metformin

Fig. 6

Composite photomicrographs of insulin immuno-reactive pancreas of non-diabetic and diabetic pigs showing normal insulin/b-cells positive stain (A), few insulin/b-cells positive stain (H&E), and near-normal insulin/b-cells positive stains (C&D). Insulin antibody stain counterstained with H&E; X250. A = pancreas of normal control pigs, B = pancreas of diabetic control pigs, C = pancreas of pigs treated with 250 mL/day Camel milk, D = pancreas of pigs treated with 500 mL/day Camel milk, E = pancreas of pigs treated with Metformin