Overweight male rats received oral
oleoyl-estrone (OE) for 10 days, and were compared with controls. The expression of
17beta-hydroxysteroid dehydrogenase (17betaHSDH)
isoenzymes, and other
proteins related to
sex hormone metabolism, were analyzed in testicle, liver, adrenals and two white adipose sites: subcutaneous inguinal and epididymal pads using a semiquantitative RT-PCR method.
Androstenedione,
testosterone,
estrone and
estradiol levels were measured by HPLC-MS/MS.
Isoenzyme expressions were grouped according to their main physiological function (oxidative or reductive) and preferred substrate (
androgen or
estrogen). As expected, testicle was the main site for synthesis of
testosterone and
estradiol, and the liver the main organ oxidizing them to
androstenedione and
estrone. Overall oxidative capacity was 6.5-fold higher than the reductive, and
estradiol synthesis and oxidation potential were higher than for
testosterone. OE decreased serum
androgens, and increased
estrone, but not
estradiol. This was due to decreased testicle ability to produce
testosterone, because of smaller size and decreased 17betaHSDH3 expression, but also to lower availability of precursors. High
estrone availability (from OE hydrolysis) does not translate into higher
estradiol because of decreased testicle reductive 17betaHSDH expression and decreased
aromatase. In consequence, we can assume that OE effects on
androgens, and the hypothalamic-pituitary-gonadal axis are limited to testicles.