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In parallel with the rapid growth of obesity, there is also an increase in the prevalence of type 2 diabetes mellitus (T2D) worldwide. Due to its complications, cardiovascular diseases are the leading cause of death in those patients. In the last two decades, special attention has been given to oxidative stress and inflammation, as the underlying mechanisms related to T2D occurrence and progression. Moreover, micro-ribonucleic acids (miRNAs) as new genetic biomarkers take an important place in the investigation of different metabolic pathways of insulin signaling. In this review article, we discuss microRNA modulation with oxidative stress and inflammation in patients with T2D. Better insight into the novel potential therapeutic targets for treatment of diabetes and its complications is of utmost importance for public health.

Introduction Markers of iron homeostasis are related to insulin resistance (IR) in adults. However, studies in children and adolescents are scarce and show contradictory results. The aim was to evaluate the potential relationship between iron status markers and IR. Additionally, no previous study has explored the mutual effect of biomarkers of iron homeostasis and inflammation (i.e. high sensitivity C-reactive protein (hsCRP)), and adipokines (i.e. retinol-binding protein 4 (RBP4)) on IR in the cohort of adolescent girls. Material and methods A total of 60 girls age between 16 and 19 years were included in the study. Serum levels of ferritin, transferrin, soluble transferrin receptor (sTfR), hsCRP, and RBP4 were measured by immunonephelometry. Homeostasis model assessment of insulin resistance (HOMA-IR) and iron homeostasis indexes were calculated. Univariate and multivariate binary logistic regression analysis were used to investigate the possible independent associations of the examined biomarkers. Principal component analysis was used to examine their mutual effect on HOMA-IR in the studied girls. Results Ferritin, sTfR, hsCRP and RBP4 were significant predictors for higher HOMA-IR in univariate analysis (p = 0.020, p = 0.009, p = 0.007, p = 0.003, respectively). Multivariate regression analysis after adjustment for waist circumference (WC) showed that serum sTfR levels remained positively associated with higher HOMA-IR (p = 0.044). Factorial analysis revealed that the obesity-inflammation related factor (i.e., WC and hsCRP) and adipokine-acute phase protein related factor (i.e., RBP4 and ferritin) showed significant differences between HOMA-IR < 2.5 and HOMA-IR ≥ 2.5. Conclusions Serum sTfR levels are independently associated with HOMA-IR, whereas higher serum ferritin levels together with higher RBP4 are related to higher HOMA-IR in adolescent girls.

Introduction We aimed to examine serum endocan level and the summary involvement of dyslipidemia, oxidative stress (OS) and inflammation by calculation of its comprehensive score (i.e. Dyslipidemia-Oxy-Inflammation (DOI) score) in relation to glucoregulation in subjects with prediabetes and overt type 2 diabetes (T2D). Material and methods A total of 59 patients with prediabetes and 102 patients with T2D were compared with 117 diabetes-free controls. Glycated hemoglobin (HbA 1c ), inflammation, OS and lipid parameters were measured. Associations of clinical data with HbA 1c level were tested with univariate and multivariate logistic ordinal regression analysis. HbA 1c as a dependent variable is given at the ordinal level (i.e. 6.4%, respectively). Results Endocan was significantly higher in the T2D group than in the controls. As endocan concentration rose by 1 unit, the probability for higher HbA 1c concentration increased by more than 3 times (OR = 3.69, 95% CI: 1.84–7.01, p < 0.001). Also, a rise in the dyslipidemia score, oxy score, inflammation score and DOI score by 1 unit increased the probability of higher HbA 1c concentration by 19%, 13%, 51% and 11%, respectively. In the models, after adjustment for confounding variables, endocan and DOI score remained independent predictors of HbA 1c level. Conclusions Endocan and DOI score are independently correlated with HbA 1c in patients with prediabetes and overt T2D.