White Tea Intake Mitigates SIRT1 Suppression in Type 2 Diabetes Skeletal Muscle: A Nutraceutical Approach to Redox Balance

Abstract

Objective: Type 2 diabetes mellitus (T2DM) impairs skeletal muscle function, reducing metabolic flexibility and mitochondrial efficiency while increasing oxidative stress due to excess reactive oxygen species (ROS) and weak antioxidant defenses. Sirtuin 1 (SIRT1) and Sirtuin 3 (SIRT3), NAD⁺-dependent deacetylases, support mitochondrial health and activate ROS-detoxifying enzymes. We hypothesized that prediabetes (PreDM) reduces SIRT1 and SIRT3 expression in muscle, contributing to redox imbalance and mitochondrial dysfunction. White tea (WTEA), known for its anti-hyperglycaemic and antioxidant properties, may counteract these effects. This study investigates the impact of PreDM on SIRT1/SIRT3 expression in rat skeletal muscle and whether WTEA supplementation offers protective benefits. Methods: All rats were provided with ad libitum access to a standard chow meal. At one month of age, the streptozotocin (STZ)-treated rats were divided into two groups: the PreDM+WTEA group (N=6) consumed white tea (WTEA) for the subsequent two months, while the other STZ-treated group (PreDM group, N=6), and the control group (control group, N=6) consumed water. Relative mRNA expression levels of SIRT1 and SIRT3 in skeletal muscle were quantified via quantitative polymerase chain reaction. Statistical significance was evaluated by one-way ANOVA, followed by Tukey post-test using GraphPad Prism 10. Results: PreDM significantly reduced mRNA SIRT1 expression in skeletal muscle. Notably, WTEA supplementation restored SIRT1 transcript levels to those comparable with non-PreDM controls. No significant differences were detected in SIRT3 expression between PreDM, WTEA-treated, and control groups. Conclusions: These findings suggest that PreDM selectively downregulates SIRT1 expression in skeletal muscle, potentially contributing to oxidative stress and metabolic impairment. WTEA supplementation appears to reverse this effect, highlighting a possible therapeutic role. In contrast, SIRT3 expression remained unchanged, indicating a possible differential regulatory response to PreDM in muscle tissue.