Camel whey protein protects B and T cells from apoptosis by suppressing activating transcription factor-3 (ATF-3)-mediated oxidative stress and enhancing phosphorylation of AKT and I?B-α in Type i diabetic mice

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Abstract

Background: Diabetes mellitus (DM) is associated with severe immune system complications. Camel whey protein (CWP) decreases free radicals (ROS) and modulates immune functions, but its effect on DM-impaired immune systems has not been studied. We investigated the impact of CWP on the immune system in a Type 1 diabetes mouse model. Methods: Three experimental groups were used: (1) non-diabetic control; (2) diabetic; and (3) CWP-treated diabetic mice. Results: Induction of diabetes by streptozotocin was associated with reduction of body weight and insulin level, increase in glucose level and pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α), and reduction in IL-2 and IL-4 levels. Upregulated ATF-3 expression was followed by a marked elevation in ROS levels. Lymphocytes from diabetic mice exhibited increased apoptosis through decreased phosphorylation of AKT and IkB-α, increased infiltration of T cells in the spleen and thymus, and decreased B cell numbers in the spleen. Supplementation with CWP decreased the levels of proinflammatory cytokines, ROS, and ATF-3 expression, and increased the levels of IL-4. Treatment with CWP decreased apoptosis by enhancing the phosphorylation of AKT and IkB-α as well as T-cell and B-cell distribution in the spleen and thymus. Conclusions: Our findings suggest the beneficial effects of CWP supplementation during diabetes on decreasing and orchestrating the redox status and subsequently rescuing the immune cells from exhaustion.

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Badr, G., Sayed, L. H., Omar, H. E. D. M., Abd El-Rahimd Ema, A. M., Ahmed, A., & Mahmoud, M. H. (2017). Camel whey protein protects B and T cells from apoptosis by suppressing activating transcription factor-3 (ATF-3)-mediated oxidative stress and enhancing phosphorylation of AKT and I?B-α in Type i diabetic mice. Cellular Physiology and Biochemistry, 41(1), 41–54. https://doi.org/10.1159/000455935

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