Study showing winstrols activity independent of A/R binding/DNA interaction...

[sterol]

I'm not so sure I agree with this. Are you saying different hormone/receptor complexes initiate transcription at different DNA locations? As far as I know, the DNA binding domains for transcription factors associated with AR/hormone homodimer are independant of the hormone bound. Or am I wrong?

Andy

No, not that they regulate diferent sites, the transduction pathway isn't going to change; AR is AR.

 

[Stew Meat]

Re: STEW- LET ME PICK YOUR BRAIN!!

Stew- at what dose does this become significant? Does the amount of increased IGF-1 come close to what you would consider an effective exergeneous IGf-1 dosage? Is the receptor increase a result of the AAS or rather the increased amount of IGF-1? In other words, if somone took exergeneous IGF-1, would they expirience the same receptor increase? Are you positive that the increase in IGF-1 is not somewhere downstream of AR activation?

I don't know what the dose at which it becomes signifigant, but the IGF-1 expression is dose dependant. Testosterone raises IGF-1 receptor concentrations directly, independent of IGF-1's activity; high IGF-1 levels will also increase IGF-1 receptor concentration. However, high levels of IGF-1 will not raise the androgen receptor concentrations. The IGF-1 increase is not understood to be related to AR function... an entirely non-AR mediated anabolic effect of testosterone. It is not known whether other androgens will have the same effect as testosterone in raising IGF-1 levels and IGF-1 receptor concentrations.

The above muscle cell IGF-1/AR expresssion experiment was done on partially aborded fetuses, btw...

The same study outlined the following: In men, Heavy resistance training leads to hypertropy which leads to increased testosterone levels. Hypertrophy can also increase IGF-1 levels slightly. But in Women, hypertrophy does NOT lead to increased testosterone levels but leads to an even higher IGF-1 concentration than with men (and control group).

I know that estrogens raise IGF-1 levels as well... What about receptor concentration?

I haven't studied estrogen to any large extent so I don't know the direct method of involvemen with it and IGF-1.



[qutoe]Also, do you feel that androgens can directly inititate tanscription of certain genes without first binding the AR(not necesarily the same sequence transcribed by the AR/steroid complex)?

Definately... hence the IGF-1 receptor increase.

The reason why 1000mg of test/week is significantly better than 500mg/week is obvioulsy because of increased AR activation... However if androgens can initiate transcription of DNA independent of the AR, that might explain the only slight benefit from going from 1000mg/week to 2000mg/week.

I agree... However, you also have to keep in mind that receptor concentration is also going to be increasing slightly...


Everything I said is backed by research.






-Stew

 

[bud 1]

I just love this board, I sure save this topic in a file, really good info Huck...

 

[cockdezl]

I am actually in total agreement with STEW on this one. I came in late, but the study cited showed NO evidence of enhancement of muscular contractile potential. In fact, the receptors that it did modulate, the benzo/GABA receptors, are neuroINHIBITORY. Who takes Xanax or Valium and then trains hard? Nobody...these drugs turn one into a zombie, due to reduction in neural transmission. If you read this study again, it states that "androgenic/anabolic steroids modulate in vitro ligand binding to the benzodiazepine binding site(s) associated with the gamma-aminobutyric acidA (GABAA) receptor complex (Masonis and McCarthy, 1995). " This means that other steroids have this ability also, thus it is not unique to stanazolol.

As for all this "Class I and Class II" classification of steroids, remember, this is not a supported classification scheme. Bill Roberts came up with this, and while as bright as he is, he is still the only one who uses this system. Pat Arnold has come out rejecting this system of classification.

The research only supports AR agonism as the major pathway of anabolic processes. And if you want to get more into it, aromatization plays a key role in GH/IGF elevations.

"I haven't studied estrogen to any large extent so I don't know the direct method of involvemen with it and IGF-1."

Estrogen increases insulin levels, as well as GH pulsatility, which both directly elevate IGF levels.

 

[OMEGA]

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[georgie24]

 

[nandi12]

Cockdezl, you are correct in stating that other AAS interact with the GABA system. The paper referenced below showed that deca and methyltest, as well as winny, interact with the GABA receptor:

J Neurophysiol 2000 Jun;83(6):3299-309
Anabolic steroids induce region- and subunit-specific rapid modulation of GABA(A) receptor-mediated
currents in the rat forebrain.

Jorge-Rivera JC, McIntyre KL, Henderson LP.

Department of Physiology, Dartmouth Medical School, Hanover, New Hampshire 03755, USA.

 

[hurricane]

good thread