Luteinizing Hormone when released actually stimulates the Leydig Cells to release testosterone.  When the blood serum levels of Testosterone or Cortisol are elevated due to hypersecretion from the adrenals, this would suppress LH (Luteinizing Hormone) I would say and in the latter (Testosterone) this means that the testicles DO shut down testosterone production, but that is because of the hypothalmus sensing the elevated levels of it in the blood serum as I had thought originally above.

This is a snippet from a page that I cut and pasted here to learn more about the Hypothalmic + Pituitary + Testis Axis for anyone concerned with male fertility. The fertility side of things has been of interest as I studied that more with writing about LOCAH. 

The page I have written has lot’s about female fertility and not a great deal about the male side of thigns so I have been researching so that I can balance that.  there is not much info out there with this regard really.  So I guess it pays to understand the reproductive physiology well and the relation to the adrenals also where problems can occur when it concerns CAH.

When we did our projects in Biology at school, that was always the topic I enjoyed the most!  I did my project on Reproduction!  I think that that is why I have been more interested in that side of things and the way it affects not just males from utero to adulhood but also women with CAH in utero to adulthood. 

So you were right I feel about the testicular production of testosterone shutting down Melissa. Which brings me to estrogen...nevermind..next time. :)

This is the URL I got this info from:

 
http://physiology.pnb.sunysb.edu/hby531/BY32/Lec%2022_00.htm

 

IV.          Endocrine Regulation of Male Reproductive Function

 

Overview:  The process of spermatogenesis and all other aspects of male reproductive function depend on the presence of hormones produced by the hypothalamus, the anterior pituitary, and the testis forming what is known as the hypothalamic-pituitary-testis axis (Fig. 8 =Tortora and Grabowski, 9th edition, 28.9).  Failure of any component of this system will result in infertility, loss of secondary sex characteristics, and if occurring embryonically failure to develop into a male.  Furthermore, this axis is subject to feedback regulation through which the various hormones levels are controlled.  We will now consider each component in turn.

 

2.  The Hypothalamus:  Certain neurons of the hypothalamus release gonadotropin releasing hormone (GnRH) into the hypothalamic-pituitary portal system where it then travels to the anterior pituitary to affect the secretion of pituitary hormones called gonadotropes.

 
3.  Anterior Pituitary: Cells of the anterior pituitary called gonadotropes respond to GnRH by increasing secretion of two hormones called follicle stimulating hormone (FSH) and luteinizing hormone (LH).  These hormones, together known as gonadotropins are released into the blood stream where they circulate to end in the testis to interact with their respective target cells.

 
4. Testis:  The target cells for gonadotropins are:

Leydig cells:  are the target cell for LH and in response increase their secretion of testosterone.  Some of this testosterone remains locally to affect Sertoli cells, whereas much of it is released into the blood stream where it circulates to affect other organs of the male reproductive system as well as other tissues and organs. 
Sertoli cells  are the target cell for FSH and in response increase functions which support spermatogenesis.  Actually testosterone from Leydig cells and FSH together result in a number of changes such as an increase in the amount of androgen binding protein (which chaperones testosterone to developing spermatocytes and throughout the male reproductive tract) and increases in metabolic support to spermatocytes.
 

5. Feedback Regulation:  Testosterone inhibits release of GnRH from the hypothalamus and LH release from the pituitary.  Interestingly, it does not affect FSH secretion at the level of the pituitary, and only does so indirectly by its effect on GnRH.  Instead FSH secretion is inhibited by a regulatory molecule released from Sertoli cells called inhibin.

 

6.  Effect of Androgens:  Testosterone and other androgens interact with a large variety of target cells, but all function by combining with an intracellular receptor called the androgen receptor.  In some target cells, the testosterone is converted to another potent androgen called dihydrotestosterone (DHT) in a process catalyzed by an enzyme called 5a reductase.  DHT interacts with the same androgen receptor, which functions by combing to the target cell DNA and affects gene transcription.  Among the effects of androgens in the body are:

Development of the male internal and external genitalia in embryonic and fetal development.
Development of male secondary sexual characteristics (beard, deep voice, etc)
Anabolism of various tissues such as an increase in muscle and bone mass, etc.
Development of sexual function: including stimulating spermatogenesis and supporting male sex drive (libido). 
 

HERE IS A QUESTION AND ANSWER FROM ANOTHER WEB SITE:

Q:  How does Trioxalon differ from Andro 100 and DHEA?
 
  
A:  Its pathway for increasing testosterone differs from both Androstenedione 100 and DHEA.

Trioxalon 500 exerts its testosterone elevating effect through the increase in luteinizing hormone (LH). LH is responsible for "telling" your body to produce testosterone. One interesting fact: Steroids suppress LH, thus reducing and sometimes shutting down your body’s production of testosterone. Trioxalon 500 counters this side effect very effectively.
 
YOU’LL FIND THAT HERE:

http://www.ast-ss.com/Products/ProductAnswer.asp?ProdID=24&QAID=146