The relationship between stathmin-2 level and metabolic parameters in newly diagnosed type 2 diabetes mellitus patients

Background: Stathmin is a phosphoprotein that plays a role in intercellular and intracellular signaling, inflammation, and differentiation. Our aim was to evaluate the stathmin-2 level and its relationship with the metabolic parameters of newly diagnosed type 2 diabetes mellitus (nT2DM) patients. Material and method: This case-control study included 76 patients with nT2DM and 76 healthy individuals with a normal oral glucose tolerance test who were matched for body mass index (BMI), age, and gender. In addition to laboratory and anthropometric measurements related to type 2 diabetes mellitus (T2DM), stathmin-2 levels were determined using an enzyme-linked immunosorbent assay. Results: We observed significantly higher circulating stathmin-2 levels in subjects with T2DM compared to the control group (6.39 +/- 1.60 ng/mL and 4.66 +/- 0.80 ng/mL, p<0.0001). In patients with metabolic syndrome, circulating stathmin-2 levels were significantly elevated compared to those without metabolic syndrome in both the T2DM and control groups (T2DM: 7.16 +/- 1.24 vs 5.06 +/- 1.24 ng/mL, p<0.001; Control: 3.84 +/- 1.40 vs 3.82 +/- 1.40 ng/mL). In both groups, we observed a positive correlation between stathmin-2 levels and BMI and circumference. Moreover, stathmin-2 showed a positive correlation with high-sensitivity C-reactive protein (hs-CRP), homeostatic model assessment of insulin resistance, insulin, fasting blood glucose, hemoglobin A1c, BMI, low-density lipoprotein cholesterol, and total cholesterol. A negative correlation was observed with stathmin-2 and high-density lipoprotein cholesterol. Stathmin-2 did not show any correlation with age, triglyceride, and lactate dehydrogenase. Conclusions: Stathmin-2 levels were found to be elevated in patients with nT2DM and exhibited positive correlations with hyperinsulinaemia, hyperglycaemia, HOMO-IR and hs-CRP levels. These results indicate that stathmin-2 may play a role in T2DM pathogenesis.