Correlation between adipokines and mediators of non-specific inflammation in type 2 diabetic patients depending on...

Introduction: The relationship between glycaemic control in type 2 diabetes and the risk of its complications has been proven in many studies. However, the role of adipose tissue hormones and non-specific inflammatory mediators in type 2 diabetes compensation has not been studied completely. The aim: To evaluate the correlation between the content of selected adipose tissue hormones and mediators of nonspecific inflammation, depending on the glycemic control in type 2 diabetes.

Materials and methods: the study has been focused on the analysis of contents and correlations between leptin, resistin, IL-2, IL-6, TNF-α in 305 patients with type 2 diabetes, who were divided into the following groups (according to their glycemic control): group 1 - with optimal glycaemic control (HbA1c ≤ 7%), group 2 - with suboptimal glycaemic control (HbA1c 7.1-8%), and group 3 - with poor glycaemic control (HbA1c ≥ 8.1%).

Results: the group of type 2 diabetic patients with poor glycaemic control showed a higher resistin level compared with the patients with optimal (+29.43%; <0.05) and suboptimal glycaemic control (+33.45%, < 0.05). Statistically, when comparing groups of type 2 diabetic patients with the different glycaemic control we have noticed no significant changes in the leptin concentration (all > 0.05). The level of circulating insulin was significantly lower in the group of type 2 diabetic patients with poor glycemic control of diabetes, compared to those with suboptimal glycaemic control (-20.87%; <0.05).

Conclusions: In patients with type 2 diabetes an impaired glycaemic control does not influence the leptin level. Though impaired glycaemic control significantly raises resistin level in the blood serum. Studying the concentration of cytokines (TNF-α, IL-2 and IL-6) in the blood serum of type 2 diabetic patients showed that glycaemic control does not provoke any significant differences in their content. The study has proved that resistin is more closely interconnected to cytokines in case of worsening the diabetes compensation - there has been found a significant positive correlation between the content of TNF-α and resistin in the group with optimal glycaemic control, then between IL-6 and resistin in the group with suboptimal glycaemic control; and in the group with unsatisfactory glycaemic control there has been detected a correlation between TNF-α, IL-2, IL-6 and resistin.