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The aim of the present study was to estimate risk factors for type 2 diabetes in women. A case–control study included 99 newly diagnosed cases of type 2 diabetes and 198 controls. Descriptive statistics were used, and conditional univariate logistic regression analysis was used to determine differences between cases and controls. According to multivariate analysis-independent risk factors for T2DM were as follows: oral contraceptives (OR = 2.57; 95% CI = 0.99–6.62), and their longer duration of use (OR = 3.55; 95% CI = 1.79–6.99); greater quantity of coffee consumed (OR = 1.89; 95% CI = 1.06–3.39), occupation (odds ratio – OR = 3.17; 95% confidence interval – CI = 1.57–6.41); never been pregnant (OR = 5.88; 95% CI = 2.23–15.49); family history of diabetes (OR = 18.52; 95% CI = 7.25–47.62); overweight and obesity (OR = 2.13, 95% CI = 1.39–4.53); stress (OR = 4.42; 95% CI = 2.19–8.26), and the greater number of stressful life event (OR = 1.65; 95% CI = 1.22–2.23). The present study emphasizes the role of oral contraceptive use, a greater quantity of coffee consumed, occupation, never been pregnant, overweight and obesity, major stressful life events, and family history of diabetes in the development of type 2 diabetes. What is already known about this topic (1) It is well known that lifestyle factors and genetics are involved in the development of type 2 diabetes mellitus (T2DM) and its complications. (2) Gender differences in T2DM are explained by differences in sex chromosomes, sex hormones, possible hormonal disbalance, lifestyle habits in nutrition, and physical activity. (3) The global prevalence of diabetes will increase to 366 million by 2030, even if the prevalence of obesity remains constant. (4) The vast majority of patients with diabetes have T2DM. (5) Knowledge of modifiable and non-modifiable risk factors for T2DM is important for the prevention of this disease. (6) Many factors have been investigated for their relation to T2DM, but data on the association between some of them and the risk for diabetes are not consistent. What this paper adds (1) Independent predictive factors for T2DM in women are oral contraceptive use and quantity of coffee consumption. (2) Other independent predictive factors for T2DM include occupation, never been pregnant, overweight and obesity, major stressful life events, and family history of T2DM. (3) A greater number of children was significantly negatively related to T2DM. (4) In this study, oral contraceptive use and especially their use for 5 years and more were significantly positively associated with T2DM after adjustment for potential confounding factors. (5) This study highlights, in particular, the need to target overweight and obese women who use oral contraceptives, have never been pregnant, and consume a greater quantity of coffee, with major stressful life events and a family history of diabetes. These groups are more vulnerable to T2DM; thus, prevention should focus on these groups. [ABSTRACT FROM AUTHOR]

The rs540467 SNP in the NDUFB6 gene, encoding a mitochondrial complex I subunit, has been shown to modulate adaptations to exercise training. Interaction effects with diabetes mellitus remain unclear. We assessed associations of habitual physical activity (PA) levels with metabolic variables and examined a possible modifying effect of the rs540467 SNP. Volunteers with type 2 (n=242), type 1 diabetes (n=250) or normal glucose tolerance (control; n=139) were studied at diagnosis and subgroups with type 1 (n=96) and type 2 diabetes (n=95) after 5 years. Insulin sensitivity was measured by hyperinsulinemic-euglycemic clamps, oxygen uptake at the ventilator threshold (VO2AT) by spiroergometry and PA by questionnaires. Translational studies investigated insulin signaling and mitochondrial function in Ndufb6 siRNA-treated C2C12 myotubes, with electronic pulse stimulation (EPS) to simulate exercising. PA levels were 10 and 6%, VO2AT was 31% and 8% lower in type 2 and type 1 diabetes compared to control. Within 5 years, 36% of people with type 2 diabetes did not improve their insulin sensitivity despite increasing PA levels. The NDUFB6 rs540467 SNP modifies PA-mediated changes in insulin sensitivity, body composition and liver fat estimates in type 2 diabetes. Silencing Ndufb6 in myotubes reduced mitochondrial respiration and prevented rescue from palmitate-induced insulin resistance after EPS. A substantial proportion of humans with type 2 diabetes fails to respond to rising PA with increasing insulin sensitivity. This may at least partly relate to a polymorphism of the NDUFB6 gene, which may contribute to modulating mitochondrial function. Clinical Trial Registration: ClinicalTrials.gov, identifier NCT01055093. The trial was retrospectively registered on 25th of January 2010. [ABSTRACT FROM AUTHOR]

Aims: To describe in a real‐world setting the achievement of physician‐selected individualized HbA1c targets in individuals with type 2 diabetes, newly or recently initiated with basal insulin, and the association of hypoglycaemia with target achievement. Materials and methods: A 12‐week, prospective, single‐arm, observational study of adults with type 2 diabetes, either newly initiated with any basal insulin or start on basal insulin within the preceding 12 months. At enrollment, eligible participants from 28 countries were treated with or without oral antihyperglycaemic drugs and/or GLP‐1 receptor agonists. Results: Individualized targets for almost all of the 3139 evaluable participants (99.7%) had been set by their physicians, with 57% of participants having HbA1c targets between 7.0% and <7.5% (53 and <58 mmol/mol). By week 12, 28% and 27% of newly and previously initiated participants, respectively, achieved individualized HbA1c targets with modest average increases in daily insulin dose of 9 and 5 U (0.10 and 0.06 U/kg), respectively, from baseline (14 and 23 U [0.17 and 0.29 U/kg], respectively). Overall, 16% of participants experienced at least one episode of hypoglycaemia. Both the incidence and frequency of hypoglycaemia, but not the severity, were positively associated with a higher likelihood of achieving individualized HbA1c targets (P < 0.05). Conclusions: In this prospective real‐world study, most participants using basal insulin did not achieve the individualized HbA1c targets set by their physicians. Participants who experienced symptomatic hypoglycaemia were more likely to achieve HbA1c targets than those who did not. [ABSTRACT FROM AUTHOR]

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Background: Galectin-3 is a protein widely distributed in the heart, brain and blood vessels, and has a regulatory role in inflammation, immunology and cancer. Many studies demonstrated that the increased level of galectin-3 is associated with progressive fibrosis and stiffening of the myocardium. The aim of this study was to investigate the role of galectin-3 in patients with type 2 diabetes (T2D) and/or arterial hypertension (HT). Methods: Study population included 189 patients, with no coronary artery disease, divided into three groups: group 1 (T2D), group 2 (T2D+HT), and group 3 (HT). All subjects underwent routine laboratory tests, as well as specific biomarkers assessment [galectin-3, glycosylated hemoglobin (HbA1c), N- terminal fragment B-type natriuretic peptide (NT-proBNP)]. Cardiological evaluation included physical examination, transthoracic tissue Doppler echocardiography and stress echocardiography. Results: The results of this study demonstrated significantly increased levels of galectin-3, blood glucose, and HbA1c in group 2. Also, echocardiographicaly, left ventricular (LV) diameters and IVS thickness were increased in this group of patients. Furthermore, in the same cohort a positive correlation between galectin-3 and NT-pro BNP, and galectin-3 and LV mass were demonstrated. In addition, a negative correlation between galectin-3 and LV end-diastolic diameter was revealed. Conclusions: This study revealed that levels of galectin-3 were higher in patients with both T2D and HT, and correlated with LV mass, indicating the potential role of this biomarker for early detection of myocardial structural and functional alterations. [ABSTRACT FROM AUTHOR]

Type 2 diabetes (T2D), one of the most prevalent noncommunicable diseases, is often preceded by insulin resistance (IR), which underlies the inability of tissues to respond to insulin and leads to disturbed metabolic homeostasis. Mitochondria, as a central player in the cellular energy metabolism, are involved in the mechanisms of IR and T2D. Mitochondrial function is affected by insulin resistance in different tissues, among which skeletal muscle and liver have the highest impact on whole-body glucose homeostasis. This review focuses on human studies that assess mitochondrial function in liver, muscle and blood cells in the context of T2D. Furthermore, different interventions targeting mitochondria in IR and T2D are listed, with a selection of studies using respirometry as a measure of mitochondrial function, for better data comparison. Altogether, mitochondrial respiratory capacity appears to be a metabolic indicator since it decreases as the disease progresses but increases after lifestyle (exercise) and pharmacological interventions, together with the improvement in metabolic health. Finally, novel therapeutics developed to target mitochondria have potential for a more integrative therapeutic approach, treating both causative and secondary defects of diabetes. [ABSTRACT FROM AUTHOR]

In recent years, many studies have revealed the importance of heart failure (HF) development in type 2 diabetes (T2D), which increases the morbidity and mortality during the course of diabetes. In this context, it became important to emphasize the role of both cardiologists and diabetologists in the early diagnosis and further adequate treatment of HF in T2D. While HF appears in two major forms, with reduced or preserved ejection fraction (EF), namely HFrEF and HFpEF, it became important to define the optimal approach to the diagnostics. Regarding HFrEF, the role of cardiological methods remained dominant, while the complexity of early diagnosis requires nowadays more active participation of diabetologists. The absence of abundant symptoms and echocardiographic findings imposed the need for the use of risk markers based on metabolic variables and low-grade inflammation parameters. Following that unmet need, numerous studies have defined the possible relationship between metabolic variables in diabetes and the risk for HF. Moreover, attempts have been made to integrate biochemical and clinical parameters into risk score engines and some of them gave promising results. However, the follow-up studies in T2D subjects are needed to determine the clinical relevance of these new approaches. [ABSTRACT FROM AUTHOR]