Aim The aim of our study was to assay circulating interleukin-15 (IL-15) and interleukin-6 (IL-6) levels and insulin resistance measured by two different methods in newly diagnosed autoimmune diabetes (AD) patients, their I° relatives, and healthy controls. Material and Methods The group studied consisted of 54 patients with AD (28 with Latent Autoimmune Diabetes in Adults (LADA) and 26 with type 1 diabetes (T1D)), 70 first-degree relatives, and 60 controls. IL-6, IL-15, and anti-islet antibodies concentrations were measured by ELISA method. Homeostatic model assessment-insulin resistance (HOMAIR) and estimated glucose disposal rate (eGDR) were calculated. Results The patients with AD had significantly higher IL-15, IL-6, and HOMAIR and lower eGDR than the controls (p < 0.001, respectively) and first-degree relatives (p < 0.001, respectively). Significantly higher IL-15 and IL-6 were shown in the relatives with positive Ab as compared to the relatives without antibodies (p < 0.001, respectively) and the controls (p < 0.001, respectively). IL-15 negatively correlated with eGDR (r = −0.436, p = 0.021) in LADA and positively with HOMAIR in LADA and T1D (r = 0.507, p < 0.001; r = 0.4209, p < 0.001). Conclusions Significantly higher IL-15 and IL-6 concentrations, HOMAIR, and markedly lower eGDR in newly diagnosed AD patients and first-degree relatives with positive anti-islet antibodies might suggest the role of these pro-inflammatory cytokines and insulin resistance in the pathogenesis of autoimmune diabetes. IL-15 and IL-6 might be used as biomarkers of the risk of autoimmune diabetes development, in particular IL-15 for LADA. Both methods of IR measurement appear equally useful for calculating insulin resistance in autoimmune diabetes.

Due to many adverse effects of gestational diabetes mellitus (GDM) on the mother and fetus, its diagnosis is crucial. The presence of GDM can be confirmed by an abnormal fasting plasma glucose level (aFPG) and/or oral glucose tolerance test (OGTT) performed mostly between 24 and 28 gestational week. Both aFPG and abnormal glucose tolerance (aGT) are used to diagnose GDM. In comparison to measurement of FPG, OGTT is time-consuming, usually inconvenient for the patient, and very often needs to be repeated. Therefore, it is necessary to seek tests that will be helpful and convenient to diagnose GDM. For this reason, we investigated the differences in fasting serum metabolites between GDM women with abnGM and normal FPG (aGT-GDM group), with aFPG and normal glucose metabolism (aFPG-GDM group) as well as pregnant women with normal glucose tolerance (NGT) being a control group. Serum metabolites were measured by an untargeted approach using gas chromatography–mass spectrometry (GC–MS). In the discovery phase, fasting serum samples collected from 79 pregnant women (aFPG-GDM, n = 24; aGT-GDM, n = 26; NGT, n = 29) between 24 and 28 weeks of gestation (gwk) were fingerprinted. A set of metabolites (α–hydroxybutyric acid (α–HB), β–hydroxybutyric acid (β–HB), and several fatty acids) significant in aGT-GDM vs NGT but not significant in aFPG-GDM vs NGT comparison in the discovery phase was selected for validation. These metabolites were quantified by a targeted GC–MS method in a validation cohort consisted of 163 pregnant women (aFPG-GDM, n = 51; aGT-GDM, n = 44; and NGT, n = 68). Targeted analyses were also performed on the serum collected from 92 healthy women in the first trimester (8–14 gwk) who were NGT at this time, but in the second trimester (24–28 gwk) they were diagnosed with GDM. It was found that α–HB, β–HB, and several fatty acids were associated with aGT-GDM. A combination of α–HB, β–HB, and myristic acid was found highly specific and sensitive for the diagnosis of GDM manifested by aGT-GDM (AUC = 0.828) or to select women at a risk of aGT-GDM in the first trimester (AUC = 0.791). Our findings provide new potential markers of GDM and may have implications for its early diagnosis.

Insulin resistance is described as reduced sensitivity of the body tissues to insulin. In pregnant women insulin resistance increases during each trimester of pregnancy due to the hormones produced by the placenta and many other factors which are not yet fully recognised. Growing insulin resistance leads to an increase in beta cell mass and number and insulin secretion, which helps to maintain glucose homeostasis and normal foetal development. However, in cases of severe insulin resistance, insufficient compensation of pancreatic beta cells or reduced pancreatic beta-cell function, glycaemic levels are increased and gestational diabetes mellitus develops. The aim of the present review is to analyse the factors affecting insulin resistance and the adaptation of pancreatic beta cells during pregnancy and methods of insulin resistance assessment.

Introduction. Betatrophin is primarily produced in the liver and regulates the metabolism of triglycerides. Its elevated concentration might be associated with an increased risk of type 2 diabetes. The aim of the study was to evaluate the impact of betatrophin on beta cell function and to compare the concentration of betatrophin in patients newly diagnosed with type 1 diabetes mellitus (T1DM including LADA), type 2 diabetes mellitus (T2DM) and a control group (CG) of healthy volunteers. Patients and methods. The study included 210 patients with newly diagnosed diabetes (70 with T1DM, 140 with T2DM) and 70 CG. To evaluate the relationship between betatrophin and insulin secretion, a glucagon stimulation test was conducted. Results. Serum betatrophin concentrations were significantly elevated in T1DM and T2DM in comparison to the control group (3.47 [Q 1 = 2.28, Q 3 = 4.54] in T1DM vs. 1.81 [Q 1 = 1.04, Q 3 = 2.67] ng/ml in CG, p < 0.001; 3.12 [Q 1 = 1.89, Q 3 = 4.48] in T2DM vs. 1.81 [Q 1 = 1.04, Q 3 = 2.67] ng/ml in CG, p < 0.001). No statistically significant differences in betatrophin concentration were observed between the T1DM and T2DM groups. Significant correlations were established between betatrophin, triglyceride (TG) and high-density lipoprotein (HDL) levels in all study participants, and C-peptide in the T1DM group. Conclusions. Betatrophin concentration was significantly elevated in patients with newly diagnosed T1DM and T2DM, compared to the control group and could be a biomarker of diabetes. Our study provided evidence which supports the impact of betatrophin on lipid metabolism. The positive correlation between betatrophin and C-peptide in the T1DM group suggests that betatrophin is associated with insulin secretion in