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Fro. Prolactin, PR, Fina. Help with answers

  • Thread starter Thread starter Golfer18--old
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Growth hormone, insulin, prolactin and total thyroxine in the plasma of sheep implanted with the anabolic steroid trenbolone acetate alone or with oestradiol.

Res Vet Sci 1981 Jan;30(1):7-13 (ISSN: 0034-5288)

Donaldson IA; Hart IC; Heitzman RJ [Find other articles with these Authors]

The mode of action of the anabolic steroid trenbolone acetate (19-norandrost-4,9,11-trien-3-one-17-acetate) was studied through the endogenous hormonal response of castrated male sheep to subcutaneous implantation of 140 mg of trenbolone acetate and 20 mg of oestradiol both separately and in combination. Radioimmunoassay of delta-4,9,11-trienic steroids and oestradiol-17 beta in plasma confirmed that simultaneous administration of trenbolone acetate with oestradiol led to a significantly greater persistence of oestradiol-17 beta residues in plasma (P less than 0.05) than with implantation of oestradiol alone. Oestradiol treatment increased concentrations of growth hormone and insulin (P less than 0.05; P less than 0.001 respectively) in plasma samples collected weekly. Trenbolone acetate by itself had no significant effect and the oestrogenic response was blocked on the simultaneous implantation of trenbolone acetate and oestradiol (despite higher plasma levels of oestradiol-17 beta with this treatment). Plasma total thyroxine was markedly depressed to 45 per cent of its basal level by trenbolone acetate, alone or with oestradiol (P less than 0.001) and depressed to 80 per cent of basal by oestradiol treatment alone (P less than 0.001). Plasma prolactin was unaltered by the above treatments.
 
Quantitative bibliographic review on the use of anabolic hormones with steroidogenic action in ruminants for meat production. II. Principal mode of action]

[Revue bibliographique quantitative sur l'utilisation des hormones anabolisantes a action steroidienne chez les ruminants en production de viande. II. Principaux modes d'action.]
Reprod Nutr Dev 1993;33(4):297-323 (ISSN: 0926-5287)

Schmidely P [Find other articles with this Author]
INA-PG, station Nutrition et Alimentation, Paris, France.

The hypotheses on the modes of action of hormonal anabolic agents in growing animals have been reviewed in more than 120 recent publications. The mechanisms of action are still not fully understood. Androgens such as testosterone and estrogens such as oestradiol-17 beta (E-17 beta) may act in different ways: firstly, testosterone (and probably also E-17 beta) acts directly on different tissues, and particularly at the level of the muscle cell by binding to a specific receptor. The hormone-receptor complex interacts with the nuclear receptor located in the chromatin and enhances protein synthesis (and probably also protein degradation). Trenbolone acetate (TBA) reduces protein synthesis and to a greater extent protein degradation. This action of TBA could take place via a reduction in the activity of catabolic glucocorticoids, either by a diminution in their secretion, or by displacing them from their receptor, or by reducing the number of receptors. Secondly, an indirect action of anabolic hormones is probable via the modifications in activity of other growth-regulating hormones. Growth hormone and insulin-like growth factor-I concentrations are enhanced by E-17 beta, diethylstilbestrol, zeranol and testosterone but not by TBA. Insulin appears to be indirectly enhanced by estrogens through an increase in growth hormone, whereas androgens reduce insulin levels. Thyroid hormone (tri- and tetra-iodothyronine) activity is reduced by androgens, whereas the action of oestrogens depends on the physiological maturity of the animal. The modes of action of these anabolic hormones are discussed in relation to growth rate and body composition.
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Quadsweep said:
You are stuck Bro! glad to be of service. I have a question??? How come I answer all of you bastards questions and help you out and none of you give me karma!!!:bawling:

:worried: :FRlol: :FRlol: okay, u twisted my arm, theres ya some karma
 
so then what u are saying is that using ru-486 to lower progesterone levels will cause gyno bc progestin is able to bind and increase prolactin causing gyno right?

i am confused. is ru-486 good for preventing high progesterone and prolactin
 
Do you have any basis for this statement other than an obscure study that showed TA binding to the PR's in the uterus of cows?



WormAAA77 said:
since tren is a progestin, it's the lack of progesterone in the presence of progestin that causes these effects. vitex will fulfill that absence of progesterone which makes tren free to bind to the PR. the puffiness is likely due to prolactin which vitex obviously suppresses.
 
-Fina binds to the progesterone receptor in certain tissues
-Progesterone stimulates the production of prolactin
-Prolactin and/or estrogen are the causes of gyno
-RU-486 blocks progesterone and reduces prolactin
-Progesterone downregulates estrogen receptors
-Blocking progesterone with RU-486 upregulates the estrogen receptor
-RU-486 causes gyno.

For references see my post (nandi12) on this topic at Triedia:

http://www.triedia.com/forum/showthread.php?s=&threadid=11926
 
Maybe no relation what so ever. But when i run winny with fina i dont have problems, when i dont run winny with it, i have problems.
 
Winny may very well reduce the chances of getting gyno. What I worry about is some newbie thinking this is gospel and living to regret it.
 
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