Introduction: Several decades of basic science and animal research provided considerable support for significant role of plasma free fatty acids (FFAs) in etiology of Type 2 diabetes mellitus (T2DM). Contradicting data related to signifi cance of elevated FFAs in plasma of patients with Type 2 diabetes prompted us to study concentrations of palmitic acid, stearic acid, and linoleic acid, in patients and healthy controls in an attempt to possibly use them as potential biomarkers in progression of the disease. Since aging is associated withincreased plasma glucose and insulin levels that are consistent with an insulin resistant state, in this study,age differences in the concentration of the above mentioned acids were tested.Methods: Progressive changes in their concentrations were followed through a period 6 months. All subjects included in the study were free of evidence of hepatitis B or C viral infection or active liver and kidney damage. Analysis of glucose and glycated hemoglobin levels were performed on BT PLUS 2000 analyzer using standard IFCC protocols, while concentrations of FFAs were analyzed by gas chromatography.Results: Our data demonstrated signifi cantly higher FFA values in plasma of diabetic patients as compared to healthy controls. There was a trend of correlation of FFAs levels with the blood glucose levels in diabetic patients, which was more prominent in diabetic men than in women.Conclusion: With aging, levels of free fatty acids signifi cantly increased in plasma of diabetic patients, and this effect was also more profound in male than in female diabetics.

Introduction: The enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) catalyzes the conversion of the hormonally inactive cortisone to active cortisol, thus facilitating glucocorticoid receptor activation in target tissues. Increased expression of 11β-HSD1 in adipose tissue has been associated with obesity and insulin resistance. In this study, we investigated the association of two 11β-HSD1 gene (HSD11B1) polymorphisms with the metabolic syndrome (MetS) and its characteristics in the Bosnian population. Materials and methods: The study included 86 participants: 43 patients diagnosed with MetS and 43 healthy controls. Subjects were genotyped for two HSD11B1 gene polymorphisms: rs846910: G>A and rs45487298: insA, by the high resolution melting curve analysis. Genotype distribution and an influence of genotypes on clinical and biochemical parameters were assessed. Results: There was no significant difference in the mutated allele frequencies for the two HSD11B1 gene polymorphisms between MetS patients and controls. In MetS patients, no significant associations between disease-associated traits and rs45487298: insA were found. Regarding rs846910: G>A variant, heterozygous patients (G/A) had significantly lower systolic (P = 0.017) and diastolic blood pressure (P = 0.015), lower HOMA-IR index (P = 0.011) and higher LDL-cholesterol levels (P = 0.049), compared to the wild-type homozygotes. In the control group, rs45487298: insA polymorphism was associated with lower fasting plasma insulin levels (P = 0.041), lower homeostasis model assessment insulin resistance (HOMA-IR) index (P = 0.041) and lower diastolic blood pressure (P = 0.048). Significant differences between rs846910: G>A genotypes in controls were not detected. Haplotype analysis confirmed the association of rs45487298: insA with markers of insulin resistance in the control subjects. Conclusions: Our results indicate that a common rs45487298: insA polymorphism in HSD11B1 gene may have a protective effect against insulin resistance.

Objective: The primary goal of this study was to determine the difference of abundance of CD4+, CD8+ and CD56+ bronchoalveolar fluid’s lymphocytes and their subpopulations between cancerous lung and healthy lung from the same patient. Methods: Mini-bronchoalveolar lavage was taken from 55 patients from lung with cancer and healthy lung. After laboratory processing and addition of CD4, CD8, CD27, CD28 and CD56 antibody, the material was analyzed by flow cytometer. Results from lung with cancer were compared to the ones from the healthy lung. The examined patients were the test and the control group at the same time. Results: CD27+28+ forms of CD4+ and CD8+ lymphocytes are more activated in the cancerous lung compared to healthy lung, while the CD27-28- forms are less activated in diseased lung. CD4+ forms of CD56+ lymphocytes are more activated in cancerous lung compared to the health lung, while the CD8+ forms are less activated in diseased lung. Conclusion: Immature helper and cytotoxic T lymphocyte response, as well as regulatory NK and NKT cell response are more activated in cancerous lung compared to the health lung of the same patient.