Population mean levels show a mild total T decline, an SHBG increase, a steeper free T decline, and a moderate LH increase with important contribution of comorbidities (e.g., obesity) to these changes.
Associations of SHBG with some anthropometric and metabolic variables in FDR suggests that lower levels is a marker for risk of developing T2D through obesity dependent metabolic pathways but low FAI is a better marker of state of diabetes in males.
In a multivariate logistic regression analysis, lower peak SBP [odds ratio (OR) 1.02;95% confidence interval (CI) 1.00-1.04, P = 0.017] and rapid early rise in heart rate (OR 15.03; 95% CI 6.23-36.24, P < 0.001) were associated with a higher risk of revealed symptoms while the use of antihypertensive treatment was associated with a lower risk of revealed symptoms (OR 0.40; 95% CI 0.18-0.89, P = 0.025), independent of age, obesity, LV ejection fraction and aortic valve area.
Although SHBG SNPs associated with type 2 diabetes mellitus do not appear to be associated with PCOS status, rs1799941 and rs727428 genotypes are associated with SHBG levels independent of the effects of insulin resistance and obesity.
Also in multivariate logistic regression model, for each increase of a child in the family the risk of abdominal obesity [OR: 0.95; 95% CI: 0.91-0.97), high SBP [OR: 0.88; 95% CI: 0.81-0.95)] and generalized obesity [OR: 0.95; 95% CI: 0.91-0.99)] decreased significantly.
Metabolic component specific analysis showed that sex hormones were inversely associated with several components of MetS: TT with abdominal obesity, low high-density lipoprotein cholesterol (HDL-C) and high blood pressure; cFT with abdominal obesity and high blood pressure; SHBG with all components except high blood pressure.
Significant additive interactions with obesity or central obesity were detected for total testosterone (RERI=2.75, 95% CI=0.92,4.59), SHBG (RERI=5.71, 95% CI=0.77,10.64), and FEI (RERI=-9.96, 95% CI=-19.18,-0.74) with regard to IR, beta-cell dysfunction, and T2D.
To investigate the contribution of serum levels of testosterone (TS) and sex hormone binding globulin (SHBG) in association with body mass index (BMI) as a surrogate marker of obesity, to the predictive capability of tumor size (T), lymph node (N) and estrogen receptor (ER) status and proliferative activity (TLI).
We tested the effects of weight loss on serum estradiol, estrone, testosterone, and sex hormone-binding globulin (SHBG) in overweight/obese women 18 months after completing a year-long, 4-arm, randomized-controlled dietary weight loss and/or exercise trial.
While low circulating total testosterone concentrations in modest obesity primarily reflect reduced concentrations of sex hormone binding globulin, more marked obesity can lead to genuine hypothalamic-pituitary-testicular axis (HPT) suppression.