Oxidative stress markers and inflammation in type 1 and 2 diabetes are affected by BMI, treatment type, and complications

Abstract

Diabetes mellitus (DM) is a common global metabolic disease. Oxidative stress from reactive oxygen species (ROS) contributes to its development and leads to complications like heart disease, kidney failure, and stroke. Chronic inflammation in diabetes is associated with insulin resistance and elevated glucose levels, as indicated by increased markers of interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor-alpha (TNF-α). This study investigates the activity and concentration of antioxidant enzymes (SOD, GPX1, CAT) and inflammatory markers (IL-6, CRP, TNF-α) in patients with type 1 and type 2 diabetes compared to healthy controls. The study included 73 patients-33 with type 1 diabetes (18 men, 15 women) and 40 with type 2 diabetes (20 men, 20 women)-and 41 healthy controls (23 men, 18 women). Antioxidant enzymes and inflammatory markers were measured using enzyme-linked immunosorbent assay (ELISA), and HbA1c levels were assessed. Program R and Statistica 13 were used to analyze the results. Group membership had a significant impact on SOD and CAT activity (p < 0.0001) and GPX1 (p < 0.001). BMI correlated with CAT concentration (p < 0.0001). SOD activity was affected by comorbidities, such as arthritis and urinary tract issues (p = 0.03). Diabetes markedly altered inflammatory markers, particularly CRP and TNF-α (p < 0.0001), and higher IL-6 levels were found in patients using medications other than metformin (p = 0.01). Type 1 and 2 diabetes significantly affect antioxidant enzyme activity and concentration. High SOD and GPX activity suggests chronic oxidative stress, while increased BMI is linked to lower enzyme levels. Additionally, TNF-α levels rise with diabetes duration, which may serve as a biomarker for disease progression and complications, potentially helping to predict diabetic complications and insulin resistance.

Keywords: CAT; CRP; Diabetes type 1; Diabetes type 2; Diabetic complications; GPX; Il-6; SOD; TNFα.

Fig. 1

(a) Etiological classification of diabetes according to WHO (2023); (b) Pathomechanism of type 1 and type 2 diabetes; Created in BioRender. Cecerska-heryć, E. (2025) https://BioRender.com/undefined.

Fig. 2

Kruskal–Wallis ANOVA analysis of the SOD activity [U/ml] in the control group and the study group; p < 0.0001.

Fig. 3

U-test analysis of the SOD activity [U/ml] in the study groups in people with and without urinary tract diseases; p = 0.03.

Fig. 4

U-test analysis of the SOD activity [U/ml] in the study groups of people with joint degeneration compared to people without degeneration; p = 0.03.

Fig. 5

Kruskal–Wallis analysis of the CAT concentration (ng/ml) in subjects in the control group and subjects in the study groups, showing a significant difference between the control group and people with type 1 diabetes (p < 0.0001) and type 2 diabetes (p < 0.0001).

Fig. 6

Kruskal–Wallis analysis of the CAT activity [ng/ml] depending on BMI; p < 0.001.

Fig. 7

U-test analysis of the effect of metformin treatment on CAT concentration [ng/ml] in people with type 1 and type 2 diabetes; p = 0.02.

Fig. 8

Kruskal–Wallis ANOVA analysis of the GPX1 concentration (ng/ml) in the control and study groups; p < 0.001.

Fig. 9

U-test analysis of the effect of insulin treatment on IL-6 levels in patients with type 1 and type 2 diabetes; p = 0.05.

Fig. 10

U-test analysis of the influence of diabetic complications on IL-6 concentration [pg/ml; p = 0.02.

Fig. 11

U-test analysis of the treatment’s effect on IL-6 concentration (pg/ml) with tablets other than metformin; p = 0.01.

Fig. 12

Kruskal–Wallis ANOVA analysis of the CRP concentration [pg/ml] depending on group assignment; p < 0.0001.

Fig. 13

Kruskal–Wallis ANOVA analysis of the influence of BMI on the concentration of C-reactive protein (pg/ml) in the studied individuals; p = 0.032.

Fig. 14

Kruskal–Wallis ANOVA analysis of the relationship between TNF-α concentration [pg/ml] and group affiliation; p < 0.0001.

Fig.15

Kruskal–Wallis ANOVA analysis of the influence of BMI on the concentration of TNF-α [pg/ml] in people qualified for the study; p < 0.01.

Fig. 16

Spearman correlation strength between the levels of selected antioxidant enzymes, inflammatory markers, biochemical parameters, and other factors in the control group and the study groups.