Femara/Arimidex and fat cells

[VANIAN]

I've read on this board that Femara gets into the fat cells and stops aromatization. It's my understanding that aromatization takes place in fat cells, the liver, and even muscle. Is it feasible to come to the conclusion that Arimidex just prevents aromatization in the liver and muscle and not fat cells? And if you had a higher body fat percentage like 15% then would Femara be much more effective because more aromatization would be occuring in fat cells that arimidex would have no affect on? It seems to me that if one had a low body fat % there would be little conversion of Test to estrogen in fat cells, so arimidex and Femara would be equally effective. But with a higher body fat % Femara would be greatly more effective. Can anyone shed any light on this? Am I way off base, or do my assumptions have some credibility? Thanks for the help.

 

[justwannagetsum]

where did you read that ?

 

[VANIAN]

I read it here:

http://boards.elitefitness.com/forum/showthread.php?s=&threadid=127713&highlight=femara

I've also seen it mentioned in other posts on this board and in posts on other boards, maybe it's misinformation, but I'm sure someone can shed some light about Femara/Arimidex and fat cells though.

Here's another post:

http://boards.elitefitness.com/forum/showthread.php?s=&threadid=80976&highlight=femara+fat+cells

One more:

http://boards.elitefitness.com/forum/showthread.php?s=&threadid=49996&highlight=femara+fat+cells

and another:

http://boards.elitefitness.com/forum/showthread.php?s=&threadid=84165&highlight=femara+fat+cells

 

[nandi12]

J Steroid Biochem Mol Biol 2001 Jan-Mar;76(1-5):199-202

Intracellular aromatase and its relevance to the pharmacological efficacy of aromatase inhibitors.

Bhatnagar AS, Brodie AM, Long BJ, Evans DB, Miller WR.

Novartis Pharma AG, CH-4002, Basel, Switzerland.

An important feature of the pharmacological profile of aromatase inhibitors is the ability of the various inhibitors to inhibit intracellular aromatase. It is now well documented that a large proportion of breast tumors express their own aromatase. This intratumoral aromatase produces estrogen in situ and therefore may contribute significantly to the amount of estrogen to which the cell is exposed. Thus it is not only important that aromatase inhibitors potently inhibit the peripheral production of estrogen and eliminate the external supply of estrogen to the tumor cell, but that they in addition potently inhibit intratumoral aromatase and prevent the tumor cell from making its own estrogen within the cell. To study the inhibition of intracellular aromatase we have compared the aromatase-inhibiting potency of the non-steroidal aromatase inhibitors, letrozole, anastrozole and fadrozole in a variety of model cellular endocrine and tumor systems which contain aromatase. We have used hamsters ovarian tissue fragments, adipose tissue fibroblasts from normal human breast, the MCF-7Ca human breast cancer cell line transfected with the human aromatase gene and the JEG-3 human choriocarcinoma cell line. .Although letrozole and anastrozole are approximately equipotent in a cell-free aromatase system (human placental microsomes), letrozole is consistently 10-30 times more potent than anastrozole in inhibiting intracellular aromatase in intact rodent cells, normal human adipose fibroblasts and human cancer cell lines. Whether these differences between letrozole and anastrozole are seen in the clinical setting will have to await the results of clinical trials which are currently in progress