Evaluation of prothymosin alpha, trimethylamine-N-oxide, and ischemia-modified albumin in type 2 diabetes mellitus patients with dysregulated lipid profile.

Background: Prothymosin alpha (PTMα) is a small acidic polypeptide from the thymosin family with immune activity and protective properties against oxidative stress induced by reactive oxygen species trimethylamine-N-oxide (TMAO), produced in the liver from gut bacterial metabolite trimethylamine and associated with increased cardiovascular disease risk and higher all-cause mortality. Ischemia-modified albumin (IMA) is a significant oxidative stress biomarker, particularly in ischemia-reperfusion conditions. This study investigates PTMα, TMAO, and IMA levels in type 2 diabetes mellitus (T2DM) patients, both with and without hyperlipidemia, to explore their relationships and their potential role as biomarkers or therapeutic targets. Method: The study received ethical approval from the Selcuk University Faculty of Medicine Hospital committee under approval number 2024/33. The study included male and female T2DM patients aged 30-60, with 30 having hyperlipidemia and the rest being non-lipemic. TMAO was performed using API 3200 LC-MS\MS while PTMα was analyzed using an ELISA kit from BT LAB, serum IMA levels were evaluated by the spectrophotometric method. Results: Comparisons were made between those with T2DM and control groups. In the T2DM group, PTMα was significantly higher in females (p = 0.047), while TMAO and IMA showed no significant gender difference. The control group had no significant differences in PTMα, TMAO, and IMA levels. Comparisons among healthy controls, non-lipemic T2DM patients, and hyperlipidemic T2DM patients revealed significantly decreased PTMα levels with no change in IMA levels across groups. In contrast, TMAO was significantly higher in the patient group. Conclusion: The findings of this study have potential implications for the field, suggesting that PTMα might serve as a prognostic indicator for T2DM and that reduced TMAO levels might play a role in T2DM pathogenesis, opening up new avenues for research and treatment.