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Old 01-10-2011
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Question Exogenous testosterone causing infertility mechanism

Why does taking exogenous testosterone cause infertiliy and testicular atrophy? I understand that it causes negative feedback on gonadotrophic hormones but how come it doesn't have the same effect on the male reproductive system that naturally made testosterone does? Why is it not converted to DHT etc?

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Old 01-10-2011
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Post Sertoli cells

The Sertoli cells in testes are very selective, they only take and accept Testosterone from Leydig cell (no other source is accepted at all)
that is the main reason , plz correct me if my understanding is wrong
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Old 01-10-2011
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Info Exogenous Testosterone does not reach the seminiferous tubules

dr z, is absolutely correct.
Exogenous testosterone cannot reach the seminiferous tubules of the testis unless it's given in supraphysiologic doses with side effects such as hepatitis.
Therefore, this exogenous testosterone will work peripherally, increasing muscle mass, verilization, ...etc but it won't increase sperm counts. On the contrary it will cause feedback inhibition of the LH release which is needed for by Leydig cells to produce local testicular testosterone.
This is why Testosterone is not option for azospermin males.
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Old 05-11-2014
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How do anabolic steroids cause gynecomastia? Is it due to aromatization into estrogen?
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Old 05-15-2014
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I want to adjust some of the responses from earlier.

Dr. Z, the sertoli cells do not only accept testosterone from leydig cells. Exogenous testosterone could be chemically identical to locally produced testosterone, and it would still not help. The difference is the concentration. In local testosterone production (normal), the testes are exposed to high levels of testosterone, and the hormone diffuses out to produce normal (lower) systemic levels. By contrast, exogenous testosterone use produces normal systemic levels, but is diffusing back into the testes, meaning at best the testes will get normal systemic levels, which is too low for them.

There simply isn't enough testosterone in the testes to be converted into DHT. You might ask, well why doesn't the testes just produce more testosterone, since the local level is low? The answer is that regulation is not local. The hypothalamus and pituitary regulate testosterone production, and they see the normal systemic level, so FSH and LH decrease, inhibiting local testosterone production.

Prim, the above should answer your questions, please reply if you feel it didn't and I'll try to clarify.

Warfarin, yes, that is exactly what happens. Remember that adipose tissue has aromatase in it, and testosterone is an anabolic hormone (promotes fat and muscle formation). More fat = more aromatase. In addition, there is no DHT, which results in alteration of hair patterns and various other things.

Last edited by monkeymind90; 05-15-2014 at 09:02 AM. Reason: Clarification + answer warfarin's question
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Old 05-15-2014
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Quote:
Originally Posted by monkeymind90 View Post
I want to adjust some of the responses from earlier.

Dr. Z, the sertoli cells do not only accept testosterone from leydig cells. Exogenous testosterone could be chemically identical to locally produced testosterone, and it would still not help. The difference is the concentration. In local testosterone production (normal), the testes are exposed to high levels of testosterone, and the hormone diffuses out to produce normal (lower) systemic levels. By contrast, exogenous testosterone use produces normal systemic levels, but is diffusing back into the testes, meaning at best the testes will get normal systemic levels, which is too low for them.

There simply isn't enough testosterone in the testes to be converted into DHT. You might ask, well why doesn't the testes just produce more testosterone, since the local level is low? The answer is that regulation is not local. The hypothalamus and pituitary regulate testosterone production, and they see the normal systemic level, so FSH and LH decrease, inhibiting local testosterone production.

Prim, the above should answer your questions, please reply if you feel it didn't and I'll try to clarify.

Warfarin, yes, that is exactly what happens. Remember that adipose tissue has aromatase in it, and testosterone is an anabolic hormone (promotes fat and muscle formation). More fat = more aromatase. In addition, there is no DHT, which results in alteration of hair patterns and various other things.
dude!! which all books did u read for step1
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Old 05-15-2014
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Crossroads,
I didn't take a book oriented approach to step 1. I used 3 Qbanks (UWorld, Kaplan, and USMLERx), the Pathoma video series, and a detailed study schedule. If you PM me I'm happy to share that with you, but it is designed for a 5 week course, so I don't know if it would be useful to you.

My focus on the exam was to understand as much as possible, using the qbanks to identify weaknesses. Truth be told, I don't know if this was an effective strategy. I am taking the exam tomorrow morning, so it will be 3-4 weeks before I get results. I did get a 258 predicted score on my last NBME, so hopefully I will do well enough the get the residency I want.
Best,
Monkeymind90
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Old 05-15-2014
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Quote:
Originally Posted by monkeymind90 View Post
Crossroads,
I didn't take a book oriented approach to step 1. I used 3 Qbanks (UWorld, Kaplan, and USMLERx), the Pathoma video series, and a detailed study schedule. If you PM me I'm happy to share that with you, but it is designed for a 5 week course, so I don't know if it would be useful to you.

My focus on the exam was to understand as much as possible, using the qbanks to identify weaknesses. Truth be told, I don't know if this was an effective strategy. I am taking the exam tomorrow morning, so it will be 3-4 weeks before I get results. I did get a 258 predicted score on my last NBME, so hopefully I will do well enough the get the residency I want.
Best,
Monkeymind90
good luck!!!!!!!!!!!
youll rock it, please share the experience once you have your results.
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