DESCRIPTION

• Testosterone (T) and estradiol (E2) have important metabolic actions which are gender-specific (sex-dimorphic).
• Most T and E2 circulate bound to sex hormone-binding globulin (SHBG), a glycoprotein that regulates the amount of sex steroids available for biological action.
• Of total T, 54% weakly bound to albumin and other proteins, 44% bound to SHBG, 2% unbound (free T)[14].
• In reproductive age women, one third of T is secreted by the ovary, whereas two thirds arise from the peripheral conversion of androstenedione to T.
• Androstenedione is directly produced by the ovary but also from peripheral conversion of adrenal dehydroepiandrosterone sulfate (DHEA-S).
• Male Hypogonadism (for example, with androgen deprivation therapy for prostate cancer) is linked to the metabolic syndrome, type 2 diabetes and an increased risk for cardiovascular disease[10].
• Hyperandrogenism in women (for example, with polycystic ovarian syndrome) is linked to the metabolic syndrome, type 2 diabetes and cardiovascular disease[15]. High T in postmenopausal women is also linked to an increased risk of type 2 diabetes[9][6].
• High endogenous E2 is associated with an increased risk for type 2 diabetes in males and postmenopausal women[9][6].
• Low SHBG is a risk factor for type 2 diabetes in both males and females[5].
• A recent study suggested that women under the age of 45 years who have type 2 diabetes have three times the risk of early menopause compared to women without diabetes[2].
• Low total T may be associated with more advanced atherosclerotic disease markers in middle-aged men with type 2 diabetes[1].