To investigate the prevalence of diabetes in the Roma population in Serbia. We screened 11 urban and 8 rural Roma communities from October 2006 to May 2008 for the presence of diabetes. Blood glucose values, name, age, sex, presence of diabetes, family history, and obesity were recorded. We analyzed the data from 1465 Roma people, 953 women and 512 men (785 in urban and 680 in rural communities), with mean age of 42.42 ± 15.69 years. Abdominal obesity was present in 600 (41%) participants. Eighty seven participants (5.9%) already had diabetes and there were 76 (5.2%) newly discovered cases of diabetes type 2. Participants with diabetes were significantly older (F = 28.33; P < 0.01). Family history for diabetes was positive in a third of participants. The risk for diabetes was 3.48 times higher in participants with positive family history (odds ratio [OR], 3.47; 95% confidence interval [CI], 2.37-5.1; P < 0.01). Abdominal obesity was less frequent in healthy participants than in participants with diabetes (X2 = 32.55; P < 0.01). The risk of diabetes in participants with abdominal obesity was 2 times higher than in the non-obese (OR, 2.11; 95% CI, 1.24-3.55; P < 0.01). Diabetes was significantly more present in urban communities (X2 = 25.20; P < 0.01). The risk of developing diabetes was 3.65 times higher in participants from urban settlements (OR, 3.64; 95% CI, 1.99-6.66; P < 0.01). Prevalence of diabetes in the Roma people living in Serbia may possibly be higher than in the general population of Serbia and needs further investigation.

Objectives: Visceral fat is more harmful than subcutaneous fat. Women with high amounts of visceral fat have an increased risk of metabolic syndrome (MetS), insulin resistance and low level of serum vitamin D. Methods: This was a prospective, randomized and controlled study. Postmenopausal women (n = 101) aged 45–70 years were included. The assessed parameters were: body mass index (BMI), waist circumference (WC), 25-hydroxyvitamin D (25-OHD) status, serum insulin and HOMA-IR, bone mineral density, total fat mass, fat mass index (FMI) measured by DXA, and muscle strength. Results: Significantly lower values of 25-OHD (35.26 ± 1.61 nmol/l) were found in women with MetS compared to those without MetS (47.52 ± 3.47nmol/l) (t = 3.699; p < 0.000). A significant negative correlation was observed between 25-OHD levels and: WC (rho_WC = −0.94; p < 0.004), BMI (rho_BMI = −0.80; p < 0.002), FMI (rho_FMI = −0.31; p < 0.002) and impaired fasting glucose (IFG) (rho_IFG = −0.23_; p < 0.001). The percentage of body fat was statistically significantly higher in the group with insufficient 25-OHD (39.6%) and in the group with a deficit of 25-OHD (48.2%), compared with the maximum permitted percentage body fat of 35% for a female (t = −22.63; p < 0.002). The average hand grip strength of these moderately obese participants was 27.4 ± 4.7 kg. It was significantly lower than the normative grip strength for referent range groups (t = −21.65; p < 0.001). Conclusion: A low 25-OHD level in postmenopausal women is associated with high body fat, metabolic syndrome, low muscular strength and osteopenia.

Background/aim: Type 2 diabetes mellitus (T2D) is a complex metabolic impairment. Beta cell (BC) failure is the most challenging among its pathogenetic mechanisms. Recognizing reversible contributors to BC failure could guide individualized approach to early T2D treatment. The aim of this study was to compare early short-term insulin treatment vs. glimepiride, both added to metformin, on BC function, glycemic and lipid control, during 12-month follow-up. Patients and methods: Eighty newly diagnosed T2D patients, 30-65 years of age, presenting with HbA1c ≥ 9% were enrolled in the study. They were randomly assigned to single-month initial insulin therapy (INS) added to metformin, or to glimepiride and metformin (OAD) as only treatment. Subjects assigned to initial insulin intervention were thereafter switched to OAD. C-peptide (C-Pep) was analyzed at baseline and 2 hours after standardized test meal (STM). All subjects were STM-retested after 3 and 12 months. HbA1c, serum lipids, BMI, HOMA IR, and HOMA B were assessed over follow-up. Results: HbA1c was lower in INS vs OAD at 3-months: 6.26 ± 0.18% vs 6.78 ± 0.10% (p = 0.016), remaining so by 12 months (p = 0.056). BMI-adjusted ΔC-Pep was greater in INS vs. OAD at 3 months (4.60 ± 0.59 vs. 3.21 ± 0.34 m2/kg; p = 0.044), persisting by 12 months (4.57 ± 0.56 vs. 3.04 ± 0.34 m2/kg; p = 0.023). Average ΔC-Pep improvement from recruitment to 3 months was 100.8% in INS, vs. 51.3% in OAD. Prevalence of STM-ΔC-Pep response greater than 2.4 ng/mL had risen 3.2-fold by 12 months in the INS, vs. 2.4-fold only in the OAD group (p = 0.018). Conclusion: Early short-term insulin intervention in newly diagnosed T2D improves beta cell function more than glimepiride, both added to metformin, resulting in a superior and longer lasting glycemic and lipid control.

Although emerging evidence suggests that epigenetic mechanisms contribute to the pathogenesis and progression of type 2 diabetes mellitus (T2DM), data remain limited for patients with suboptimal metabolic control. The aim of this study was to assess global DNA methylation in patients with poorly controlled T2DM and to identify diabetes-related factors associated with DNA methylation levels. The study included 107 patients and 50 healthy controls. Global DNA methylation (5mC) was measured by UHPLC-DAD method. Pro-oxidant and antioxidant biomarkers, advanced glycation end-products, high-sensitivity C-reactive protein (hsCRP) and complete blood count were determined and leukocyte indices calculated. Patients had a significantly lower 5mC than controls (3.56 ± 0.31% vs. 4.00 ± 0.68%; p < 0.001), with further reductions observed in those with longer disease duration and diabetic foot ulcers. Oxidative stress and inflammatory biomarkers were higher in the patient group. DNA hypomethylation was associated with a higher monocyte-to-lymphocyte ratio and hsCRP, pro-oxidant–antioxidant balance, ischemia-modified albumin, and advanced oxidation protein products levels. Conversely, 5mC levels showed positive correlations with total antioxidant status and total sulfhydryl groups. Principal component analysis identified five key factors: proinflammatory, pro-oxidant, aging, hyperglycemic, and antioxidant. The pro-oxidant factor emerged as the sole independent predictor of global DNA hypomethylation in T2DM (OR = 2.294; p = 0.027). Our results indicate that global DNA hypomethylation could be a biomarker of T2DM progression, reflecting the complex interactions between oxidative stress, inflammation, and epigenetic modifications in T2DM.

Objective The LEADER trial (NCT01179048) demonstrated a reduced risk of cardiovascular (CV) events for patients with type 2 diabetes who received the glucagon-like peptide-1 receptor agonist liraglutide versus placebo. The mechanisms behind this CV benefit remain unclear. We aimed to identify potential mediators for the CV benefit observed with liraglutide in the LEADER trial.Research Design and Methods We performed exploratory analyses to identify potential mediators of the effect of liraglutide on major adverse CV events (MACE: composite of CV death, non-fatal myocardial infarction or non-fatal stroke) from the following candidates: HbA1c, body weight, urinary albumin-to-creatinine ratio (UACR), confirmed hypoglycemia, sulfonylurea use, insulin use, systolic blood pressure and LDL-cholesterol. These candidates were selected as CV risk factors on which liraglutide had an effect in LEADER such that a reduction in CV risk might result. We used two methods based on a Cox proportional hazards model, and the new Vansteelandt method designed to utilize all available information from the mediator and to control for confounding factors.Results Analyses using the Cox methods and Vansteelandt method indicated potential mediation by HbA1c (up to 41% and 83% mediation, respectively) and UACR (up to 29% and 33% mediation, respectively) on the effect of liraglutide on MACE. Mediation effects were small for other candidates.Conclusions These analyses identify HbA1c and, to a lesser extent, UACR as potential mediators of the CV effects of liraglutide. Whether either is a marker of an unmeasured factor or a true mediator remains a key question that invites further investigation.

Background: It is difficult to predict the risk of developing atherosclerotic cardiovascular disease in subjects with prediabetes and obesity. The aim of this study was to assess risk factors for coronary artery calcifications (CACs) and the development of type 2 diabetes (T2D) and coronary vascular events (CVEs) after 7 years in 100 overweight or obese persons with prediabetes, according to the baseline coronary artery calcium score (CACS). Methods: Lipids, HbA1c, uric acid, and creatinine were assessed. Glucose, insulin, and c-peptide were determined during an oral glucose tolerance test. Multi-sliced computerized tomography with evaluation of CACS was performed. After 7 years, the subjects were assessed for T2D/CVE. Results: CACs were present in 59 subjects. No single biochemical marker could predict presence of a CAC. After 7 years, T2D developed in 55 subjects (61.8% initially had both IFG and IGT). A gain in weight was the only contributing factor for T2D. Nineteen subjects developed a CVE; increased initial clustering of HOMA-IR > 1.9, LDL > 2.6, and mmol/Land TGL > 1.7 mmol/L and higher CACS were present in that group. Conclusions: No risk factors for CACs could be identified. A gain in weight is associated with T2D development, as are higher CACS and clustering of high LDL+TGL+HOMA-IR with CVEs.