29-01-2021, 04:26 AM
Hi Mike,
You came here seeking answers, so...let's see if we can help. I am perplexed why you didn't reach out to a Body Builder website...or maybe you did. But hey, if you'd like hairy boobs later on so be it.
Do keep in mind d-aspartic acid can be metabolized to estrogen via the Aromatase enzyme. And the exact way would be from cyclic adenosine monophosphate (cAMP), it's a second messenger pathway. In this scenario T is converted to E. My suggestion would be to add an aromatase inhibitor to stop the conversion to estrogen. Google Aromatase Inhibitors. An herbal version could be by adding DIM (Diindolylmethane). I am wondering how you'll handle the increase in DHT?, I'm thinking as you add chest hair you'll lose the hair on your head. Or just add a 5 alpha reductase inhibitor (5 ar inhibitor) it blocks DHT in hair and other target tissues.
Aromatase expression and role of estrogens in male gonad : a review
Serge Carreau et al. Reprod Biol Endocrinol. 2003.
Free PMC article
Abstract
The ability of the testis to convert irreversibly androgens into estrogens is related to the presence of a microsomal enzymatic complex named aromatase, which is composed of a specific glycoprotein, the cytochrome P450 aromatase (P450arom) and an ubiquitous reductase. The aromatase gene is unique in humans and contained 18 exons, 9 of them being translated. In the rat testis we have immune localized the P450arom not only in Leydig cells but also in germ cells and especially in elongated spermatids. Related to the stage of germ cell maturation, we have shown that the level of P450arom mRNA transcripts decreases, it is much more abundant in pachytene spermatocytes and round spermatids than in mature germ cells whereas the aromatase activity is 2-4 fold greater in spermatozoa when compared to the younger germ cells. Using a highly specific quantitative competitive RT-PCR method we have evidenced that several factors direct the expression of the aromatase gene in Leydig cells, Sertoli cells, pachytene spermatocytes and round spermatids, and it is obvious that promoter PII is the main one but other promoters could be concerned. In the bank-vole testis we have observed a positive correlation between a fully developed spermatogenesis and a strong immunoreactivity for both P450arom and estrogen receptor beta not only in Sertoli cells but also in pachytene spermatocytes and round spermatids. Our recent data obtained from ejaculated human spermatozoa demonstrate the presence of aromatase both in terms of mRNA and protein, and in addition, we suggest that aromatase could be involved in the acquisition of sperm motility. Indeed in men the congenital aromatase deficiency is associated with severe bone maturation problems and sterility. Together with the widespread distribution of estrogen receptors in testicular cells these data clearly show that estrogens play a physiological role in the regulation of spermatogenesis in mammals.
The promoter(s) of the aromatase gene in male testicular cells
Serge Carreau et al. Reprod Biol. 2004 Mar.
Abstract
Aromatase is the terminal enzyme responsible for estrogen biosynthesis in mammals; it is present in various testicular cells including germ cells. The aromatase gene (Cyp19) is unique in humans and its expression is regulated in a tissue and more precisely, in a cell-specific manner via the alternative use of various promoters located in the first exon. Nevertheless, there is little information concerning the regulation of the testicular aromatase especially in germ cells. This prompted us to study the control of Cyp19 gene expression and its role in the regulation of the testicular androgen/estrogen ratio. Gonadotrophins and cAMP modulate aromatase expression in somatic cells which confirms that promoter II is controlled via CRE. Moreover, we have demonstrated that in highly purified germ cells from adult rats (pachytene spermatocytes and round spermatids), transforming growth factor beta (TGFbeta) inhibited the expression of Cyp19 in both germ cell types. In contrast, tumor necrosis factor alpha (TNFalpha) stimulated Cyp19 expression in pachytene spermatocytes. The effect of TNFalpha is amplified in presence of dexamethasone. Therefore, we suggest that in germ cells, TNFalpha enhances expression of aromatase through promoter PI.4 in pachytene spermatocytes, possibly via an AP1 site upstream the GAS element, while in round spermatids TNF requires glucocorticoids as a co-stimulator to increase Cyp19 gene expression. In addition, we have shown that androgens and estrogens by themselves modulate Cyp19 gene expression in all testicular cell types studied suggesting the presence of ARE and ERE on the Cyp19 gene promoter(s). Finally, in presence of seminiferous tubules or Sertoli cell-conditioned media, aromatase transcripts are increased in both Leydig cells and germ cells suggesting that other locally produced modulators (e.g. LRH-1) are involved in the regulation of the aromatase gene expression especially in Leydig cells. Using RACE (Rapid Amplification of cDNA Ends)-PCR, we have confirmed that promoter II mainly directs expression of the aromatase gene in all testicular cell types studied in the rat. However, involvement of another promoter such as PI.4 is suggested as well.
You came here seeking answers, so...let's see if we can help. I am perplexed why you didn't reach out to a Body Builder website...or maybe you did. But hey, if you'd like hairy boobs later on so be it.
Do keep in mind d-aspartic acid can be metabolized to estrogen via the Aromatase enzyme. And the exact way would be from cyclic adenosine monophosphate (cAMP), it's a second messenger pathway. In this scenario T is converted to E. My suggestion would be to add an aromatase inhibitor to stop the conversion to estrogen. Google Aromatase Inhibitors. An herbal version could be by adding DIM (Diindolylmethane). I am wondering how you'll handle the increase in DHT?, I'm thinking as you add chest hair you'll lose the hair on your head. Or just add a 5 alpha reductase inhibitor (5 ar inhibitor) it blocks DHT in hair and other target tissues.
Aromatase expression and role of estrogens in male gonad : a review
Serge Carreau et al. Reprod Biol Endocrinol. 2003.
Free PMC article
Abstract
The ability of the testis to convert irreversibly androgens into estrogens is related to the presence of a microsomal enzymatic complex named aromatase, which is composed of a specific glycoprotein, the cytochrome P450 aromatase (P450arom) and an ubiquitous reductase. The aromatase gene is unique in humans and contained 18 exons, 9 of them being translated. In the rat testis we have immune localized the P450arom not only in Leydig cells but also in germ cells and especially in elongated spermatids. Related to the stage of germ cell maturation, we have shown that the level of P450arom mRNA transcripts decreases, it is much more abundant in pachytene spermatocytes and round spermatids than in mature germ cells whereas the aromatase activity is 2-4 fold greater in spermatozoa when compared to the younger germ cells. Using a highly specific quantitative competitive RT-PCR method we have evidenced that several factors direct the expression of the aromatase gene in Leydig cells, Sertoli cells, pachytene spermatocytes and round spermatids, and it is obvious that promoter PII is the main one but other promoters could be concerned. In the bank-vole testis we have observed a positive correlation between a fully developed spermatogenesis and a strong immunoreactivity for both P450arom and estrogen receptor beta not only in Sertoli cells but also in pachytene spermatocytes and round spermatids. Our recent data obtained from ejaculated human spermatozoa demonstrate the presence of aromatase both in terms of mRNA and protein, and in addition, we suggest that aromatase could be involved in the acquisition of sperm motility. Indeed in men the congenital aromatase deficiency is associated with severe bone maturation problems and sterility. Together with the widespread distribution of estrogen receptors in testicular cells these data clearly show that estrogens play a physiological role in the regulation of spermatogenesis in mammals.
The promoter(s) of the aromatase gene in male testicular cells
Serge Carreau et al. Reprod Biol. 2004 Mar.
Abstract
Aromatase is the terminal enzyme responsible for estrogen biosynthesis in mammals; it is present in various testicular cells including germ cells. The aromatase gene (Cyp19) is unique in humans and its expression is regulated in a tissue and more precisely, in a cell-specific manner via the alternative use of various promoters located in the first exon. Nevertheless, there is little information concerning the regulation of the testicular aromatase especially in germ cells. This prompted us to study the control of Cyp19 gene expression and its role in the regulation of the testicular androgen/estrogen ratio. Gonadotrophins and cAMP modulate aromatase expression in somatic cells which confirms that promoter II is controlled via CRE. Moreover, we have demonstrated that in highly purified germ cells from adult rats (pachytene spermatocytes and round spermatids), transforming growth factor beta (TGFbeta) inhibited the expression of Cyp19 in both germ cell types. In contrast, tumor necrosis factor alpha (TNFalpha) stimulated Cyp19 expression in pachytene spermatocytes. The effect of TNFalpha is amplified in presence of dexamethasone. Therefore, we suggest that in germ cells, TNFalpha enhances expression of aromatase through promoter PI.4 in pachytene spermatocytes, possibly via an AP1 site upstream the GAS element, while in round spermatids TNF requires glucocorticoids as a co-stimulator to increase Cyp19 gene expression. In addition, we have shown that androgens and estrogens by themselves modulate Cyp19 gene expression in all testicular cell types studied suggesting the presence of ARE and ERE on the Cyp19 gene promoter(s). Finally, in presence of seminiferous tubules or Sertoli cell-conditioned media, aromatase transcripts are increased in both Leydig cells and germ cells suggesting that other locally produced modulators (e.g. LRH-1) are involved in the regulation of the aromatase gene expression especially in Leydig cells. Using RACE (Rapid Amplification of cDNA Ends)-PCR, we have confirmed that promoter II mainly directs expression of the aromatase gene in all testicular cell types studied in the rat. However, involvement of another promoter such as PI.4 is suggested as well.