Decreased serum Testosterone in Type 2 Diabetes does not reflect intratesticular hypoandrogenism but is associated with decreased adiponectin

A strong association between low circulating serum testosterone (T) and incidence of type 2 diabetes was reported. Further, data from human and animal studies suggested a protective role for androgens against diabetes mellitus as a result of T ability to increase lean body mass and to decrease fat mass. Objectives of this study were to: 1) examine the relationship between low serum T and intratesticular T, essential for spermatogenesis, and adiponectin, produced by adipocytes, and is essential for increased insulin sensitivity, 2) determine the effect of low serum T on androgen receptor (AR) expression, essential for T action in diabetic testis, and 3) determine the estradiol (E2) level in serum as it reflects the dynamic of aromatization of T to E2 and may explain the cause of low serum T in diabetic patients. Experiments were performed in Zucker Diabetic Fatty (ZDF) rats. Ten ZDF rats (average glucose level of 600±38.4 mg/dl) and ten lean non‐diabetic controls (average glucose level of 121±2.4 mg/dl) were used. Results indicated significantly lower serum T in ZDF rats compared with their lean controls (3.0 ± 0.2 and 6.3± 1 ng/ml, respectively). Neither intratesticular T, AR mRNA, nor E2 levels were significantly altered by diabetes. Data suggested that lower serum T in type 2 diabetes does not accurately reflect intratesticular hypoandrogenism and is not necessarily caused by aromatization of T to estrogen. In contrast low serum T in diabetic rats is associated with significantly lower serum adiponectin level.