Aromatase: Full fat cells vs depleted fat cells

[xelnaga]

Does a fat cell have to be activated ( full) in order to take part in aromatase?

[PK-V]

Is your question, "if someone was weighing 250lbs (with a high bf) cut down to 200lbs and wanted to start a cycle, would his depleted fat cell cause a higher aromatization rate of androgens into estrogens compared to someone weighing 200lbs who was never overweight" (based in the theory that fat cells never die only shrink)?
or something along those line?
from my understanding, no.
because the fat cells are not active

[Bonaparte]

Short answer: yes.
More fat = more aromatase activity.
Don't make this more complicated than it has to be.

[Swifto]

Does a fat cell have to be activated ( full) in order to take part in aromatase?

In human adipose tissue aromatase activity is principally expressed in mesenchymal cells of undifferentiated preadipocyte phenotype. P450arom, a heme protein product of the CYP l9 gene, converts androstenedione to estrone.

Not just being "fat" determines aromotase activity.

The distribution of adipose tissue will also determine the amount of aromotase expression. Aromatase activity varies significantly by region, with greater expression in adipose tissue from buttocks and thighs compared to that from abdomen and breasts.

Adipose tissue-derived estrogens partition fat to subcutaneous and breast tissues, while androgens promote central or visceral fat accumulation.

Short answer: yes.
More fat = more aromatase activity.
Don't make this more complicated than it has to be.

Simply, yes.

But as you can see above, there are more variables than obvious.

[xelnaga]

Thank you vets!

[Swifto]

Further reading.



Estrogen production and action☆

Linda R. Nelson MD, PhDa, Serdar E. Bulun MDa,b
Purchase
From the Departments of Obstetrics and Gynecologya and Molecular Genetics,b University of Illinois at Chicago.

Available online 23 May 2002.
Abstract

Estradiol production is most commonly thought of as an endocrine product of the ovary; however, there are many tissues that have the capacity to synthesize estrogens from androgen and to use estrogen in a paracrine or intracrine fashion. In addition, other organs such as the adipose tissue can contribute significantly to the circulating pool of estrogens. There is increasing evidence that in both men and women extraglandular production of C18 steroids from C19 precursors is important in normal physiology as well as in pathophysiologic states. The enzyme aromatase is found in a number of human tissues and cells, including ovarian granulosa cells, the placental syncytiotrophoblast, adipose and skin fibroblasts, bone, and the brain, and it locally catalyzes the conversion of C19 steroids to estrogens. Aromatase expression in adipose tissue and possibly the skin primarily accounts for the extraglandular (peripheral) formation of estrogen and increases as a function of body weight and advancing age. Sufficient circulating levels of the biologically active estrogen estradiol can be produced as a result of extraglandular aromatization of androstenedione to estrone that is subsequently reduced to estradiol in peripheral tissues to cause uterine bleeding and endometrial hyperplasia and cancer in obese anovulatory or postmenopausal women. Extraglandular aromatase expression in adipose tissue and skin (via increasing circulating levels of estradiol) and bone (via increasing local estrogen concentrations) is of paramount importance in slowing the rate of postmenopausal bone loss. Moreover, excessive or inappropriate aromatase expression was demonstrated in adipose fibroblasts surrounding a breast carcinoma, endometriosis-derived stromal cells, and stromal cells in endometrial cancer, giving rise to increased local estrogen concentrations in these tissues. Whether systemically delivered or locally produced, elevated estrogen levels will promote the growth of these steroid-responsive tissues. Finally, local estrogen biosynthesis by aromatase activity in the brain may be important in the regulation of various cognitive and hypothalamic functions. The regulation of aromatase expression in human cells via alternatively used promoters, which can be activated or inhibited by various hormones, increases the complexity of estrogen biosynthesis in the human body. Aromatase expression is under the control of the classically located proximal promoter II in the ovary and a far distal promoter I.1 (40 kilobases upstream of the translation initiation site) in the placenta. In skin, the promoter is I.4. In adipose tissue, 2 other promoters (I.4 and I.3) located between I.1 and II are used in addition to the ovarian-type promoter II. In addition, promoter use in adipose fibroblasts switches between promoters II/I.3 and I.4 upon treatments of these cells with PGE2 versus glucocorticoids plus cytokines. Moreover, the presence of a carcinoma in breast adipose tissue also causes a switch of promoter use from I.4 to II/I.3. Thus there can be complex mechanisms that regulate the extraglandular production of estrogen in a tissue-specific and state-specific fashion.

(J Am Acad Dermatol 2001;45:S116-24.)

Add testes to the above list in males.