28-06-2015, 03:25 AM
Here's a rather technical look at new a developing theory (estrogen secreted in male testes)
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Sertoli cells synthesize estradiol 17b from testosterone, and when testosterone is introduced with FSH (Follicle-stimulating hormone) it produced a 12 fold increase in E2 synthesis. And is markedly increase when cAMP (Cyclic adenosine monophosphate) is also added. Estrogen also triggers rapid activation of classical second messengers (cAMP, calcium, and inositol triphosphate). On another note, FSH and cAMP produce a 30 fold increase in aromatase, quite possibly making it the strongest aromatase.
Follicle-stimulating hormone stimulates estradiol-17f synthesis in cultured Sertoli cells. (testis/testosteronemetabolism/aromatizingenzyme/cyclicAMP/seminiferoustubules)
http://www.pnas.org/content/72/7/2677.full.pdf
Although aromatase level per adipose tissue fibroblast may be small, the sum of estrogen arising from billions of adipose tissue fibroblasts in the entire body makes a physiologic impact. The principal product of the ovary is the potent estrogen estradiol. In adipose tissue, estrogenically weak estrone is produced from androstenedione of adrenal origin in relatively large quantities. However, at least half of this peripherally produced estrone is eventually converted to estradiol in extraovarian tissues.
Molecular Bases and Phenotypic Determinants of Aromatase
http://downloads.hindawi.com/journals/ije/2012/584807.pdf
Physiological regulation of aromatase expression. FSH induces aromatase expression via a cAMP-dependent pathway in ovarian granulosa cells via promoter II. SF-1 mediates this action of FSH. On the other hand, a combination of a glucocorticoid and a member of the class I cytokine family induces aromatase expression in skin and adipose tissue fibroblasts via promoter I.4 located 73 kb upstream of the coding region. Binding of STAT-3 and glucocorticoid receptor (GR) upstream of promoter I.4 mediates regulation of aromatase expression in these fibroblasts adipose tissue becomes the major aromatase-expressing body site after menopause
http://pharmrev.aspetjournals.org/content/57/3/359/F4.expansion
___________________________
Sertoli cells synthesize estradiol 17b from testosterone, and when testosterone is introduced with FSH (Follicle-stimulating hormone) it produced a 12 fold increase in E2 synthesis. And is markedly increase when cAMP (Cyclic adenosine monophosphate) is also added. Estrogen also triggers rapid activation of classical second messengers (cAMP, calcium, and inositol triphosphate). On another note, FSH and cAMP produce a 30 fold increase in aromatase, quite possibly making it the strongest aromatase.
Follicle-stimulating hormone stimulates estradiol-17f synthesis in cultured Sertoli cells. (testis/testosteronemetabolism/aromatizingenzyme/cyclicAMP/seminiferoustubules)
http://www.pnas.org/content/72/7/2677.full.pdf
Although aromatase level per adipose tissue fibroblast may be small, the sum of estrogen arising from billions of adipose tissue fibroblasts in the entire body makes a physiologic impact. The principal product of the ovary is the potent estrogen estradiol. In adipose tissue, estrogenically weak estrone is produced from androstenedione of adrenal origin in relatively large quantities. However, at least half of this peripherally produced estrone is eventually converted to estradiol in extraovarian tissues.
Molecular Bases and Phenotypic Determinants of Aromatase
http://downloads.hindawi.com/journals/ije/2012/584807.pdf
Physiological regulation of aromatase expression. FSH induces aromatase expression via a cAMP-dependent pathway in ovarian granulosa cells via promoter II. SF-1 mediates this action of FSH. On the other hand, a combination of a glucocorticoid and a member of the class I cytokine family induces aromatase expression in skin and adipose tissue fibroblasts via promoter I.4 located 73 kb upstream of the coding region. Binding of STAT-3 and glucocorticoid receptor (GR) upstream of promoter I.4 mediates regulation of aromatase expression in these fibroblasts adipose tissue becomes the major aromatase-expressing body site after menopause
http://pharmrev.aspetjournals.org/content/57/3/359/F4.expansion