Quote:
Originally Posted by 1ainslie  My T levels are at max range or over and my DHT is 2 to 3 times max level, however my Androstanediol-gluc level is only 1/3 up range. My doc says to take a lot more T as and the high DHT is not a problem because the Androstanediol-gluc is the metabolite of testosterone and is the more important level to get in the upper third, does anyone know about this? |
I thought that Androstandediol glucuronide is (most prominently) a metabolite of
DHT, not T???
There is 3-Alpha Androstandediol glucuronide and 17-Beta Androstandediol glucuronide. I think the major pathway is T -> DHT ->
DHT gluceronide (metabolisation)... if I understand it correctly. But I can be wrong; I'm no expert.
See this link for more info.
iHOP - Origin of plasma androstanediol glucuronide in men. Origin of plasma androstanediol glucuronide in men.
Moghissi E, Ablan F, Horton R
The role of
testosterone (T) and dihydrotestosterone (
DHT) as precursors of the peripheral metabolite androstanediol glucuronide (3 alpha diol G) in plasma from normal men was studied. An apparent steady state of both putative precursors and the steroid glucuronides were attained by 8-h constant iv infusions of 3H-labeled steroid after a loading dose. The unconjugated steroids and the steroid glucuronides (after beta-glucuronidase hydrolysis) with 14C indicator were purified by serial microcolumn and paper chromatography steps previously reported to achieve radiochemical purity. The specific activities of 3 alpha diol and 3 alpha diol G in plasma were widely different in each subject, confirming our earlier suggestion that the two peripheral metabolites are formed in different pools. The conversion ratios (CRPre-Prod BB) varied widely. The CRT-3 alpha diol G was generally less than 5%, while the CRDHT-3 alpha diol G was 10 times higher. These results are compatible with the expected model, T----
DHT----3 alpha diol G. In some of the studies, T glucuronide (TG) and
DHT glucuronide (DHTG) were isolated after T infusions, and DHTG was isolated after
DHT infusion. The major conversion product of blood T was DHTG, not TG, and the major conversion product of
DHT was 3 alpha diol G. This suggests that metabolism proceeds through a steroid reduction step and glucuronidation. The peripheral pathway to 3 alpha diol G may involve formation of DHTG and then 3 alpha-reduction to 3 alpha diol G. This may also explain why blood levels of unconjugated 3 alpha diol have not been helpful in elucidating disorders of androgen formation, as this androgen mostly arises from sites different from 3 alpha diol G.
J. Clin. Endocrinol. Metab. (1984)
PMID: 6746859