[quote]buffd_samurai wrote:
In the body, specifically the leydig cells in the testes, 17beta-HSD3 is the enzyme responsible for conversion of androstenedione to testosterone. In the heyday of prohormones back in the early 2000’s, I always wondered if there was a way to upregulate this enzyme to help with the conversion of either natural or exogenous androstenedione.
Same thing with 4-androstenediol which uses the 3beta-hydroxysteroid dehydrogenase (3beta-HSD)enzyme…how does one upregulate this?
Green tea and dark chocolate apparently contain high amounts of epicatechin that upregulates 17beta-HSD3, but I have not found any information or anecdotal evidence that intake of these substances significantly affected testosterone levels.
Anyone do any research in this area?[/quote]
Probably not what you are looking for:
[i]
Mol Med. 2011;17(7-8):657-64. doi: 10.2119/molmed.2010.00143. Epub 2011 Feb 22.
Steroidogenic enzymes and stem cell markers are upregulated during androgen deprivation in prostate cancer.
Pfeiffer MJ1, Smit FP, Sedelaar JP, Schalken JA
Abstract
Considerable levels of testosterone and dihydrotestosterone (DHT) are found in prostate cancer (PCa) tissue after androgen deprivation therapy. Treatment of surviving cancer-initiating cells and the ability to metabolize steroids from precursors may be the keystones for the appearance of recurrent tumors. To study this hypothesis, we assessed the expression of several steroidogenic enzymes and stem cell markers in clinical PCa samples and cell cultures during androgen depletion. Gene expression profiles were determined by microarray or qRT-PCR. In addition, we measured cell viability and analyzed stem cell marker expression in DuCaP cells by immunocytochemistry. Seventy patient samples from different stages of PCa, and the PCa cell line DuCaP were included in this study. The androgen receptor (AR) and enzymes (AKR1C3, HSD17B2, HSD17B3, UGT2B15 and UGT2B17 ) that are involved in the metabolism of adrenal steroids were upregulated in castration resistant prostate cancer (CRPC). In vitro, some DuCaP cells survived androgen depletion, and eventually gave rise to a culture adapted to these conditions. During and after this transition, most of the steroidogenic enzymes were upregulated. These cells also are enriched with stem/progenitor cell markers cytokeratin 5 (CK5) and ATP-binding cassette sub-family G member 2 (ABCG2). Similarly, putative stem/progenitor cell markers CK5, c-Kit, nestin, CD44, c-met, ALDH1A1, α2-integrin, CD133, ABCG2, CXCR4 and POU5F1 were upregulated in clinical CRPC. The upregulation of steroidogenic enzymes and stem cell markers in recurrent tumors suggests that cancer initiating cells can expand by adaptation to their T/DHT deprived environment. Therapies targeting the metabolism of adrenal steroids by the tumor may prove effective in preventing tumor regrowth.[/i]
But here is something useful:
[i]DNA Cell Biol. 2011 Sep;30(9):661-9. doi: 10.1089/dna.2010.1192. Epub 2011 May 12.
Butyrate induces expression of 17β-hydroxysteroid dehydrogenase type 1 in HT29 and SW707 colorectal cancer cells.
RawÅ?uszko AA1, Krokowicz P, JagodziÅ?ski PP.
Author information
Abstract
Epidemiological studies have revealed that butyrate and 17β-estradiol (E2) may decrease the incidence of colorectal cancer (CRC). In peripheral tissue, E2 can be produced locally by 17β-hydroxysteroid dehydrogenase 1 (HSD17B1) estrone (E1) reduction. Using quantitative real-time polymerase chain reaction and western blotting analysis, we found that sodium butyrate significantly upregulates HSD17B1 long and short transcripts and protein levels in HT29 and SW707 CRC cells. Chromatin immunoprecipitation analysis showed that upregulation of these transcript levels correlated with an increase in binding of Polymerase II to proximal and distal promoters of HSD17B1. Moreover, we observed that upregulation of HSD17B1 protein levels was associated with increased conversion of E1 to E2 in HT29 and SW707 CRC cells. Since sodium butyrate increases the conversion of E1 to E2, our findings may support the validity of butyrate in the prophylaxis of CRC incidence.[/i]
Note that something as simple as sodium butyrate in vitro increases HSD17B1.
BUT…that you can’t eat butyrate and get that effect, and
the enzyme acts to increase the production of estrone to estradiol.
There ain’t no free lunch.