(20-03-2015, 10:33 AM)-Clelia- Wrote: thank you Lotus, I'm ready to go. Happy me!
yep you gave to a scientist a good homework. How come, am I the only one? Where are all the others? There is a lot of people here. Anyway, you could be a scientist. Meanwhile I leave to you something as well, that I think you will appreciate (if you havent already read them).
" The Androgen Receptor in Breast Tissues " www.ncbi.nlm.nih.gov/pmc/articles/PMC3404296/ (2012) " Differential effects of exogenous androgen and an androgen receptor antagonist in the peri- and postpubertal murine mammary gland." www.ncbi.nlm.nih.gov/pubmed/21846805 (2011)
bye, see you soon
Wow thanks Clelia,
You've got me motivated now...
from those research papers it led me to research posted below, and from that I see DHT is non-aromatizable as we know.....but!!!!......it also create what's known as a second estrogen effect, ER-b mostly though...(pretty cool huh?). I knew it has this back-door effect, and mostly from 3b-doil. and then it would by mostly brain, bone etc end result, but none the less it does have an ER result. Now Sertoli cells on the other hand has a huge aromatase link, by way of spermatozoa.
Estrogen and androgen receptors: Regulators of fuel homeostasis and emerging targets for diabetes and obesity
http://www.ncbi.nlm.nih.gov/pmc/articles...247852.pdf
Metabolic effects of ERα and ERβ activation in females
Activation of ERα in the central nervous system (CNS) suppresses food intake, increases energy expenditure and decreases body weight. In addition, activation of ERα improves peripheral energy and glucose homeostasis in multiple ways by 1) preventing liver steatosis, suppressing hepatic glucose production and improving insulin sensitivity, 2) enhancing skeletal muscle lipid oxidation, GLUT4 expression and insulin sensitivity, 3) enhancing subcutaneous white adipose tissue (WAT) distribution while decreasing overall WAT mass by decreasing WAT free fatty acid (FFA) uptake, lipid synthesis and increasing lipolysis, 4) favoring pancreatic β-cell survival and function by preventing pro-apoptotic injuries and lipotoxicity, and increasing insulin biosynthesis and glucose-stimulated insulin release (GSIS). Activation of ERβ in the central nervous system (CNS) also suppresses food intake and increases energy expenditure and prevents obesity on a high fat diet. In addition, activation of ERβ affects peripheral energy and glucose homeostasis by 1) favoring pancreatic β-cell survival and function by preventing pro-apoptotic injuries and increasing GSIS, 2) preventing obesity and decreasing WAT mass, 3) promoting insulin resistance in absence of ERα activation. ERα and ERβ metabolic actions on peripheral tissues result from direct activations of ERs in these tissues or from a central ER action affecting peripheral tissues via the autonomous system CNS ERs.
I'll post the DHT target tissues illustration , (way cool)
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And on ther hand---from the study you listed:
Differential effects of exogenous androgen and an androgen receptor antagonist in the peri- and postpubertal murine mammary gland.
Conclusion-
Our findings indicate that androgen signaling influences development and structure of the adult mammary gland and that homeostasis between estrogen and androgen signaling in mature glands is critical to constrain the proliferative effects of estradiol.
http://www.ncbi.nlm.nih.gov/pubmed/21846805#
This is really intriguing (specifically) this statement.
Quote:flutamide treatment from 12-21 wk increased ductal branching (P = 0.004)
Which I gather (flutamide, AR) does have an impact on side branching.
(20-03-2015, 10:33 AM)-Clelia- Wrote: thank you Lotus, I'm ready to go. Happy me!
yep you gave to a scientist a good homework
Did i?..... cool, I thought I might have insulted you lol.
(20-03-2015, 10:33 AM)-Clelia- Wrote: How come, am I the only one? Where are all the others? There is a lot of people here.
Don't know....but I'm glad you're here. I have all kinds of crazy ideas and only myself to entertain them, lmao.
(20-03-2015, 10:33 AM)-Clelia- Wrote: Anyway, you could be a scientist.
You think so?, nah....... I'm not worthy
although I'd love to be one.
and thank you so much for saying so.