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http://www.ncbi.nlm.nih.gov/pubmed/8473413

Androstanediol glucuronide production in human liver, prostate, and skin. Evidence for the importance of the liver in 5 alpha-reduced androgen metabolism.

Rittmaster RS, Zwicker H, Thompson DL, Konok G, Norman RW.

Department of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada.
Abstract

Androstanediol glucuronide (Adiol G) has been reported to be a marker of peripheral androgen metabolism and action. It consists of two isomers, Adiol 3-G and Adiol 17-G. Adiol G is formed from unconjugated precursors by the enzyme glucuronyl transferase. To determine the likely source of Adiol G formation in man, we developed a glucuronyl transferase assay and measured the activity of this enzyme in human liver, abdominal and scalp skin, and prostate. In human liver, glucuronyl transferase activity was linear with respect to time (up to 120 min) and tissue concentration (up to 1 mg/ml). Apparent Michaelis-Menten constant Km (micromolar) and maximum velocity (Vmax) (picomoles per mg/30 min) were 5.6 and 140 for dihydrotestosterone, 8.9 and 1300 for androstanediol, and 3.1 and 46 for androsterone, respectively. Conversion of androstanediol to Adiol G (/0.5 mg tissue.30 min) was 5.8-13.2%. Over 80% of the Adiol G formed in human liver was Adiol 17-G, similar to what has been previously found in human serum. Glucuronyl transferase activity was present at low levels in human prostate (conversion of androstanediol to Adiol G was 0.04-4.6%/50 mg tissue.120 min). Analogous conversion rates (/50 mg tissue.120 min) for human scalp skin were 0.2-0.4% and for human abdominal skin were 0.07-0.14%. Although dihydrotestosterone may be converted to androstanediol in peripheral tissues such as skin and prostate, our results suggest that the principal site of androgen conjugation to glucuronic acid is the liver. The present results cast doubt upon the role of androstanediol glucuronide as a specific marker of cutaneous androgen metabolism.

Is this significant?

Maybe this is the reason why drinking alcohol reduces ones ability extremely to perform, and in cases of post-finasteride one gets really hammered with drinking, at least this happens to me. But what increases the activity of gluconyl transferase ???

Some people reported improvement by using liver detoxifiers like silymarin but for me it didn't work i only took it for a few days though and quit due to pains in testicles. It seems that anything i take affects my testicles

This female rats, but found it interesting

Triiodothyronine and estradiol increase the serum level of androstanediol glucuronide but do not influence androgen UDP-glucuronyl transferase activity in the female rat.

Abstract

In this study, adult female rats were treated with either estradiol, testosterone or triiodothyronine (T3). The mean +/- SD for serum levels of androstane-3 alpha,17 beta-diol glucuronide (ADIOL-G) in rats injected with estradiol (31.1 +/- 6.1 nmol/l) and T3 (28.7 +/- 6.1 nmol/l) increased three-fold in comparison to the controls (9.2 +/- 3.6 nmol/l; p < 0.01). There was no significant increase in ADIOL-G levels in rats injected with testosterone (12.0 +/- 3.4 nmol/l) even though serum testosterone levels increased more than 17-fold (1.2 +/- 0.3 nmol/l; p < 0.01). Testosterone levels remained below the detection level of the assay (0.07 nmol/l) in the control and the estradiol and T3 treatment groups. Androgen UDPGT activity in liver microsomes was not altered by treatment with testosterone, estradiol or T3. However, the UDPGT activity for p-nitrophenol increased two-fold in estradiol and T3-treated females (p < 0.01), but was not significantly altered by testosterone treatment. These results suggest that the activity of androgen UDPGT in liver is not the limiting factor in the increased serum levels of ADIOL-G observed on treatment with estradiol and T3.

http://www.ncbi.nlm.nih.gov/pubmed/8076904

People who dont respond well to HRT have to look at the liver and or other hormones?