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Project X (hrt)

(21-10-2015, 04:10 AM)eloise614 Wrote:  Yay for being hired to work at your boob-growing super lab on a resort island. Daiquiris to celebrate?! Big Grin

Lotus, if progesterone has been observed to upregulate prolactin synthesis, perhaps I should really add some pc cream.

I think so. Take a look a what prolactin can do in the nucleus (kicks DHT's ass) Big Grin

Prolactin influences upon androgen action in male accessory sex organs.
Thomas JA, Keenan EJ.
Abstract
The hormones of the pituitary gland are capable of directly influencing the function of male accessory sex organs. Among these hormones, prolactin in particular has been observed to enhance consistently the effects of androgens in the prostate gland and/or the seminal vesicles of rats, mice, and guinea pigs as well as in the accessory sex organs of other species. Prolactin-mediated augmentation of testosterone's effects upon these tissues is related primarily to the growth-promoting influences of this steroid. However, under certain experimental conditions, the androgen-dependent production of secretions by these organs has also been enhanced by prolactin treatment. Studies in the mouse have indicated that prolactin primarily enhances the proliferative phase of androgen action in male accessory sex tissues. Testosterone stimulation of RNA synthesis was unaffected by simultaneous administration of prolactin. The mechanism by which prolactin causes enhanced androgen responses in the prostate gland and seminal vesicles is not well understood. It would appear, however, that prolactin neither stimulates increased accumulation of androgen into the accessory sex organs, nor does it enhance the conversion of testosterone to the more "active" androgen, dihydrotestosterone. The effects of prolactin on these tissues are, however, dependent upon the presence of dihydrotestosterone. Uncertain, at present, are the possible effects of prolactin on the binding or retention of androgens (dihydrotestosterone?) in the prostate gland or in the seminal vesicles. There is evidence that hypophysectomy reduces the nuclear binding of dihydrotestosterone in the cells of the prostate gland. Perhaps prolactin is a pituitary factor(s) which is important in regulating nuclear binding of dihydrotestosterone in male accessory sex organs. The direct influences of prolactin upon androgen action in the cells of the accessory sex organs may involve several sites of action (Figure 2). For example, it is currently understood that when testosterone enters the cell cytoplasm it is subsequently converted to the more "active" androgen, dihydrotestosterone (DHT), by reduction at the 5alpha position. Dihydrotestosterone is then either bound to a cytoplasmic "receptor" protein (Rc) or is further metabolized to either 5alpha-androstane-3alpha,17beta-diol or 5alpha-androstane-3beta,17beta-diol (DIOL). The binding of DHT to its cytoplasmic receptor protein results in translocation of the steroid-receptor complex into the nucleus where presumably the complex dissociates and DHT exerts its androgenic effects. The transport of DHT to the nucleus can also result from the conversion of testosterone to DHT by nuclear membrane-bound 5alpha-reductase. Prolactin augmentation of DHT effects is envisioned as resulting from interaction of prolactin with its receptor, which due to the large size of the prolactin molecule is probably located in or on the plasma membrane...

remember what I said about 5alpha-androstane-3alpha,17beta-diol or 5alpha-androstane-3beta,17beta-diol (DIOL)? it can be influenced as estrogen by way of DHEA.
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Prolactin stores breast fat by increasing the production of lipoprotein lipase (LPL, a fat storage enzyme). So we also know prolactin increases the number of ER's, which kind however (ER alpha or beta) is less known.

From what I've seen in scientific literature on the different types of breast receptors it's a mix, being of 20% androgen receptors, 20% estrogen receptors, 20% glucocorticoid receptors, 20% prolactin, the rest I'm thinking its insulin (IGF-1, or IL-1) receptors. Here's the thing, too much estrogen stimulation doesn't address other receptors. It would appear that androgen receptors will inhibit breast growth by way of DHT, which is present in breast tissue, especially in skin fibroblasts. Progesterone cream is a 5 alpha reduction inhibitor, but..it also stores fat too, and helps build ductal side branching. Breast massage agents should address the receptor types. Therapy should include a 5 AR inhibitor 1st, then go with an E2 source followed by a GH source. Prolactin should could by way of nipple stimulation, have fun.
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I wish biochem was this much fun in grad school.
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(23-10-2015, 03:58 AM)L^te Bloomer Wrote:  I wish biochem was this much fun in grad school.

Lol, here's to having fun. Wink thanks LB


Question: how does a breast mature?,

Answer: with progesterone. In other words, no areola growth means breasts haven't matured yet. Proceed to check out lane with a 3:1 ratio of progesterone to estrogen supplementation. Tongue
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It is time lotus used his extensive knowledge and create a concoction and cream for marketing . Will sell like hot cakes Wink
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FOUR DAYS TO GO Sad
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(20-10-2015, 11:33 PM)Lotus Wrote:  * * *
T-minus 11 days, I'll miss posting research no one gets RolleyesBig Grin

I have been out of the loop, I guess. Can you fill me in about the "T-minus 11 days"? I enjoy not understanding, so please, please keep confusing me!
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That makes two of us Spanky
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(27-10-2015, 09:47 PM)elainecd Wrote:  That makes two of us Spanky

Lotus is officially out of here as a full time mod this Sat. Oct 31st so he can devote more time to research. SadAngry
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(27-10-2015, 10:23 PM)iaboy Wrote:  
(27-10-2015, 09:47 PM)elainecd Wrote:  That makes two of us Spanky

Lotus is officially out of here as a full time mod this Sat. Oct 31st so he can devote more time to research. SadAngry

He may quit as moderator , but still pop in to throw new found gems at us Smile
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