(The FASEB Journal. 2008;22:lb109)
© 2008 FASEB
Decreased serum Testosterone in Type 2 Diabetes does not reflect intratesticular hypoandrogenism but is associated with decreased adiponectin
Mahmoud Mansour,
Laura Stewart,
Elaine Coleman,
Tim Braden,
Benson Akingbemi,
Robert Judd,
John Dennis,
Eric Plaisance and
Edward Morrison
Anatomy, Physiology & Pharmacology, Auburn University, Auburn, AL
ABSTRACT
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.
