Tracking Sirtuin 3 in Diabetic Children: A Bioinformatics and Clinical Approach to Cellular Metabolism

Background: Sirtuin 3 (SIRT3) is the main mitochondrial deacetylase that modifies the biochemical reactions of diverse proteins within mitochondria through lysine deacetylation. This enzyme is essential for regulating mitochondrial respiratory functions, redox homeostasis, reactive oxygen species detoxification, and insulin response across various organs. SIRT3 deficiency has been linked to mitochondrial dysfunction with insufficient ATP production, which both contribute to aging and metabolic disorders such as type 2 diabetes mellitus (T2DM), insulin insensitivity, and cardiovascular complications.Aim: The present study aimed to assess serum SIRT3 levels in children with type 1 diabetes mellitus (T1DM). Materials and Methods: This study involved 90 children, divided into 45 children with T1DM and 45 healthy individuals as controls. A full medical history was taken, and biochemical tests such as fasting blood glucose (FBG), HbA1c, and lipid profile were performed. Serum levels of SIRT3 were also measured in both groups using the sandwich ELISA technique. A bioinformatic analysis was performed to explore SIRT3 structure, function, and diabetes-related networks. Results: Serum SIRT3 levels were markedly decreased in diabetic children, with significant differences between the two groups in FBG, HbA1c, triglycerides (TAG), and very low-density lipoprotein cholesterol (VLDL-C). Bioinformatics revealed that SIRT3 and its interactome are involved in diabetes-related pathways and processes. Conclusion: This research suggests that SIRT3 may be related to the pathophysiology of the disease, and that identifying the complex interplay between SIRT3 and mitochondrial function in DM could aid in developing more advanced treatment strategies.