Introduction The main objective of this research was to evaluate the association of insulin resistance (IR) with micro- and macrovascular complications, sex hormones, and other clinical data. Methods Cross-sectional study of patients older than 18 years old with type 1 diabetes mellitus (T1DM) was performed. Participants filled in questionnaires about T1D, disease duration, smoking, glycemic control, chronic diabetes complications, and hypertension status. Data about chronic diabetic complications (neuropathy, retinopathy, and nephropathy) were collected from medical records. History of major cardiovascular events such as angina, myocardial infarction, and stroke were collected from medical records also. Laboratory tests including creatinine, cholesterol levels, testosterone (T), sex hormone-binding globulin (SHBG), estradiol levels, and albumin in 24-h urine sample were performed. IR was calculated using the following formula: estimated glucose disposal rate (eGDR) = 24.31 − [12.22 × waist-to-hip ratio (WHR)] − [3.29 × hypertension status (defined as 0 = no, 1 = yes)] − [0.57 × glycated hemoglobin (HbA1c)]. The data was considered statistically significant at p < 0.05. Results A total of 200 people (mean age 39.9 ± 12.1 years) with T1D were included in the study. Patients with T1D were analyzed according to eGDR levels stratified by tertiles. The cutoff value of eGDR which reflects IR was less than 6.4 mg kg⁻¹ min⁻¹. When eGDR was less than 6.4 mg kg⁻¹ min⁻¹, diabetes microvascular complications occurred significantly more often (p < 0.001); the cutoff of eGDR for cardiovascular disease (CVD) events was less than 2.34 mg kg⁻¹ min⁻¹. Lower eGDR, longer diabetes duration, and lower HbA1c significantly increased CVD outcomes risk. eGDR was also significantly lower in smokers (7.3 ± 2.5 vs. non-smokers 8.2 ± 2.6, p = 0.011), the obese (lean 8.25 ± 2.47 vs. obese 5.36 ± 2.74, p < 0.000), older patients (less than 50 years 8.0 ± 2.5 vs. more than 50 years 6.2 ± 2.8, p = 0.001), men (men 6.4 ± 2.4 vs. women 8.7 ± 2.2, p < 0.001), patients with long-standing diabetes (< 10 years 7.3 ± 2.6 vs. > 10 years 8.7 ± 2.3, p < 0.001), and chronic diabetes complications (diabetic retinopathy, diabetic nephropathy, diabetic neuropathy, p < 0.001), and patients with CVD (with CVD 5.5 ± 2.4 vs. no CVD 8.0 ± 2.4, p < 0.001). Patients with T1D and a family history of T2D were not susceptible to weight gain during intensive insulin treatment. Metabolic syndrome (MS) phenotype prevalence, including and dyslipidemia rate, were higher in the obese group than in normal weight, but a clear difference was not seen (p = 0.07). Positive linear correlation between men’s T and eGDR level was observed (r = 0.33, p = 0.04), i.e., men with higher testosterone level had better insulin sensitivity. Other parameters (like T in women, estrogens, SHBG) did not show any significant association with eGDR. Conclusions According to stratified eGDR, IR was found for one-third of the current T1D population. Insulin resistant patients more frequently had microvascular complications and CVD events. Lower eGDR, longer diabetes duration, and lower HbA1c significantly increased CVD outcomes risk. IR was related to smoking, obesity, gender, age, and diabetes duration. Moreover, men’s testosterone had a positive correlation with IR in T1D. Finally, patients with T1D and a positive family history of T2D were not susceptible to weight gain, while MS metabolic phenotype prevalence tended to be higher in obese than in lean patients with T1D, with a tendency to significant difference.

Background: As the diagnostic and treatment options for diabetes improve, more attention nowadays is being paid to the exact identification of the etiopathological mechanism of type 2 diabetes (T2DM). Insulin resistance (IR) is a pathogenetic background for T2DM. Several studies demonstrate that miRNAs play an important role in systemic inflammation and thus in T2DM pathogenesis. Overexpression of miR-107 may cause an imbalance of glucose homeostasis, obesity, and dyslipidemia, by regulating insulin sensitivity through the insulin signaling pathway. Methods: 53 patients with T2DM and 54 nondiabetic patients were involved in the study. This study aimed to examine whether miR-107 expression in the serum of patients with diabetes was different from the control group (non-diabetic) and whether miR-107 expression correlated with lipid levels, BMI, and other factors, and finally, with insulin resistance in general. Results: miR-107 expression was higher in the T2DM group than in the control group (1.33 versus 0.63 (p = 0.016). In general, miR-107 expression was directly and positively associated with BMI (r = 0.3, p = 0.01), age (r = 0.3, p = 0.004), and male gender (p = 0.006). Moreover, miR-107 was related to dyslipidemia: Patients with higher miR-107 levels had lower HDL levels (in the control group: r = −0.262, p = 0.022 vs. diabetic group: r = −0.315, p = 0.007). Finally, the overexpression of miR-107 was associated with higher HOMA-IR in the diabetic group (r = 0.373, p = 0.035). Conclusion: MiR-107 expression is higher among diabetic patients than that of nondiabetic control subjects. Higher miR-107 levels are also related to dyslipidemia (lower HDL levels)—in the general cohort and non-diabetic subjects. Moreover, higher miR-107 expression is related to insulin resistance in the diabetic group. In general, higher miR-107 expression levels are related to a higher BMI, older age, and the male gender.

Background and objectives: Although the role of insulin in the periphery is well understood, not as much is known about its multifactorial role in the brain. The aim of this study is to determine whether exogenous insulin, evaluated by daily insulin requirement, has an impact on mild cognitive impairment (MCI), and whether this relationship is mediated by insulin doses and other risk factors. Materials and methods: A sample of 100 participants with type 2 diabetes aged 40 and over was divided into case and control groups, according to their insulin requirement. Patients with an insulin requirement >1 IU/kg/day were assessed as the case group whereas those with an insulin dose <1 IU/kg were used as the control group. All participants underwent cognitive testing using MoCA questionnaire scoring and blood analysis to determine lipid and uric acid levels in plasma. Subjects were categorized as having normal cognitive function or MCI. Results: Results showed that the prevalence of MCI in Lithuanian elderly diabetic patients was high in the groups with a normal insulin requirement or high insulin requirement at 84.8% and 72.5%, respectively (p = 0.14). Age (p = 0.001) and insulin dose (p < 0.0001) were related to the MCI. Using ROC curve analysis, the highest rate risk of MCI occurred when the insulin dose was lower than 144 IU/d. Conclusions: In summary, the results of this study provided evidence that increased exogenous insulin supply improves cognitive function. Higher insulin dose (>144 IU/d) demonstrated a positive effect on cognitive function, especially in individuals with poorly controlled diabetes (HbA1c ≥ 9%). Finally, the prevalence of MCI in the T2DM population was found to be very high. Future research is needed to determine whether high exogenous insulin doses have a protective effect on MCI.