Recently, it has been suggested that the osteoblast-specific protein osteocalcin is central in the cross-talk between bone remodeling and energy metabolism (1–3). There were no statistically significant differences between carriers and non-carriers in previously reported clinical risk factors for incident type 2 diabetes and the cigarette smoking status at baseline (p ≥ 0.05) (table 1). These effects may be mediated by modulation of intracellular calcium concentrations, stimulation of insulin gene transcription, and/or insulin receptor expression (4–7). We used multivariable logistic regression models to assess the relationship of androgen deprivation therapy exposure (2 or fewer years, greater than 2 years or none) with incident diabetes and cardiovascular disease, adjusting for age at diagnosis, race, stage and comorbidity. The primary outcome was incident ASCVD events, self-reported annually and adjudicated by blinded local and central physicians. Results: The adjusted hazard ratio for the NCEP definition was 4.62 (95% confidence interval [CI]: 3.90-5.48) and that for the IDF definition was 4.59 (95% CI: 3.84-5.50). The AACE definition had the highest sensitivity for predicting diabetes (men: 0.61; women: 0.58) and lowest specificity (men: 0.71; women: 0.70).
Pairwise interaction analysis showed that the co-occurrence of high BMI and high SAD was associated with the highest diabetes incidence, with a relative risk of 37.0 (11.2–122). Smoking history was obtained using a questionnaire developed from the third National Health and Nutrition Examination Survey (NHANES III), the National Health Interview Survey (NHIS) and the Atherosclerosis Risk in Communities Study (ARIC). Only a few studies have shown data on the incidence rate of Type 2 diabetes in relation to maintaining metabolically healthy obesity over time [15,16]. Incidence of diabetes was significantly higher in patients with uncontrolled (8%) than in those with controlled blood pressure (4%, odds ratio 2.08, P < 0.0001). An assay has been developed to measure plasma copeptin (copeptin), the C-terminal portion of the AVP precursor.