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Need a Reference on estrogen & A2 receptors

fawnmarie

New member
Can anyone give me a reference to online information on the effect of estrogen on the density of A2 receptors - something that ISN'T a website trying to sell something and is simple enough for an idiot (or a 2-month endocrinology student) to understand?

Everything I find is either a commercial or WAAAYYYY over this person's head.


Fawn
 
Not sure there is an absolute answer to your question. Although estrogens and progesterone may be associated with differences in site-specific fat accumulation in women and sex hormones may influence the activity (most likely, the number) of the adrenergic receptors on fat cells, this has not yet been confirmed in humans. Sex hormones also influence fat and carbohydrate metabolism throughout the body, which can have indirect influences on fat accumulation and breakdown. Also, sex steroids may not be the only hormones that explain site- and gender-related differences in fat accumulation. There is some evidence that catecholamine levels differ at rest and during stress in women and men. Bearing in mind that catecholamines regulate the rate of fat breakdown/accumulation in adipose tissue, such variations in catecholamine levels may contribute to other regulatory factors (such as blood circulation).

In other words, too much estrogen/not enough test may indeed lead to a relative increase in A2 receptors over B2 in women, but it is not clear that this is a direct genomic effect of estrogen on A2 receptor density. For instance, the opposite appears to be true in men-ie too much T/lack of E can also cause a relative overabundance of A2, but in the abdominal area instead of the gluteo-femoral region. Loss of estrogen (such as menopause) also causes a shift in the balance of A2:B2 receptors in the abdominal area of women. Confused??
 
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MS said:


In other words, too much estrogen/not enough test may indeed lead to a relative increase in A2 receptors over B2 in women, but it is not clear that this is a direct genomic effect of estrogen on A2 receptor density. For instance, the opposite appears to be true in men-ie too much T/lack of E can also cause a relative overabundance of A2, but in the abdominal area instead of the gluteo-femoral region. Loss of estrogen (such as menopause) also causes a shift in the balance of A2:B2 receptors in the abdominal area of women. Confused??

insulin issue not an alpha2 with respect to abdominal fat in males...

notably there has been an increase in this androgenic pattern among certain females.. likely due to a low fat diet and alcohol consumption.
 
with respect to A2 and estrogen agree that evidence is limited... and conflicting depending on animal model and tissue..


it may be more of an issue that women have so few beta receptors in comparison that even low to moderate A2= near complete inhibition of lipolysis.

its all ratios..
 
"it may be more of an issue that women have so few beta receptors in comparison that even low to moderate A2= near
complete inhibition of lipolysis.

its all ratios.."

Agreed. Even before you're born, a female has more fat cells in the butt and thigh region, and these cells are low in B2 receptors from the get-go. Changes in estrogen due to ovarian production at menarche may just lead to global changes in metabolism (including insulin sensitivity issues, which increases LPL activity in A2 dense cells) that makes these cells easier to fill with fat and more resistant to fat loss. On top of that, you also have paracrine effects from estrogen produced in areas that are already high in subQ fat....this estrogen is produced locally (due to higher aromatase activity) that acts locally (to increase more fat storage) creating a viscious circle of which the A2 receptors are just one factor.

Macro-why would a low fat diet with alcohol increase androgenic abdominal fat in women??? In general, moderate alcohol consumption and a low saturated fat diets are associated with IMPROVED insulin sensitivity of the visceral adipocytes????
 
MS said:

Macro-why would a low fat diet with alcohol increase androgenic abdominal fat in women??? In general, moderate alcohol consumption and a low saturated fat diets are associated with IMPROVED insulin sensitivity of the visceral adipocytes????

low fat = high carb

alcohol decreases insulin sensitivity in the abdominal area (the research seems to show its tissue specific)..


the fat issue, at least during development affects hormone levels.. still looking into this. but dietary fat content affects time at which menstrual cycle begins (though one must keep in mind the influence of exogenous estrogens.. which has lowered this age across the board).. and led to skyrocketing infertiliy rates in both men and women...

am willing to venture a guess that xenoestrogens are a big problem in england.. as IVF is HUGE there.
 
I guess you must mean excess alcohol (as in alcoholism or binge drinking) and diets high in sucrose/fructose/low in fiber??? Certainly a diet including moderate alcohol and low in fat, high in complex carbs is very protective against abdominal obesity and insulin resistant syndromes.

Clearly, high insulin levels lead to high T levels which lead to increased visceral fat in both men and women. Unfortunately for many women, an increase in insulin stimulated T does NOT lead to a decrease in estrogenic fat....they just end up with a big belly AND fat thighs :( I see a LOT of this happening now in very young women, and I have no doubt it is related to shitty diet (more likely high in McDonald's saturated fat and coke), excess alcohol, lack of exercise and high estrogen levels from a young age.
 
MS said:


Clearly, high insulin levels lead to high T levels which lead to increased visceral fat in both men and women. Unfortunately for many women, an increase in insulin stimulated T does NOT lead to a decrease in estrogenic fat....they just end up with a big belly AND fat thighs :( I see a LOT of this happening now in very young women, and I have no doubt it is related to shitty diet (more likely high in McDonald's saturated fat and coke), excess alcohol, lack of exercise and high estrogen levels from a young age.

differ slightly with respect to evaluation of mechanism.. however agree completely with the rest..
 
MS -

No, not confused at all - or moreso than most people who look at this closely.

Animal studies are fine for reference - if anyone knows anything about it.

Otherwise - de nada.

:)

Fawn
 
Why animal studies?? Maybe you could tell us what EXACTLY you want to know about A2 and estrogen. After all, there isn't any other animal on the planet (not even primates) who have the gluteofemoral fat distribution (in other words estrogenic fat) of a human female. There are lots of studies, but assimilating them into a BIG PICTURE based on the pervasive local, peripheral, and CNS effects of the ever-changing balance of estrogen:test:progesterone:cortisol:insulin:thyroid blah blah blah and how this leads to a relative excess of A2 receptors over B2 receptors in the butt of an adult female is not something you will find in a single or even handful of human research articles. Estrogen does not directly cause an increase in A2 receptors as far as I know, but it certainly causes a global change in amount and sensitivity to a range of lipogenic and lipolytic hormones.

Put another way, a female's breast tissue is predominantly composed of estrogen-induced fat stores, yet it is very low in A2 density.
 
No - all I really wanted to know was if there was actually any research done on the A2/estrogen connection. Tried finding the information myself and just ran into a great deal of rodent abuse. So... I was hoping someone else had already seen data on the connection and could direct me to it.

When you typed: "Although estrogens and progesterone may be associated with differences in site-specific fat accumulation ....... of the adrenergic receptors on fat cells, this has not yet been confirmed in humans. "

I had just assumed that there might have been some animal testing involved (since it hadn't been "confirmed in humans").

No big deal - if there are no studies drawing a correlation between the two, then there ARE none - and I can live with that. I understand that it's a bit more complicated than that - but really I only was looking for some reference for the correlation.


:)

Fawn
 
If you check out some of these studies:

http://www.ncbi.nlm.nih.gov:80/entr...d=Display&dopt=pubmed_pubmed&from_uid=2823049

You will probably come to the realization that a large part of the difference between fat accumulation in men and women is due to estrogen's inhibition of thyroid activity versus testosterone's ability to increase thyroid function. Gluteal-femoral fat is particularly sensitive to these changes. This results in differing numbers and sensitivities of alpha and beta adrenocreceptors between the sexes. I misundestood your original question because I thought you had read somewhere that estrogen directly affects the density of A2-ARs via genomic effects, which is not supported by any research in humans, and research in animal models is meaningless because of the lack of this female fat-distribution pattern outside of us lucky humans!

Now what was that about xenoestrogens Macro???? Have you been hitting the pesticides too much over the Christmas/New Year period :P
 
I was more interested in actual pattern of distribution in women, rather than comparing total amount with that of men.

The pattern of fat distribution in women varies a great deal, and wondering how much of this is caused by estrogen, how much by skeletal proportion, and any other factors possible factors.

Apparently I have too much time on my hands. :)

Thanks for the link, will check it out ASAP.

Fawn
 
In a nutshell, high E/low T equals PEAR SHAPE
High T/Low E equals APPLE SHAPE
High T/high E equals fat in both places (eg PCOS)

These relative fat distributions don't seem to reflect absolute A2 density so much as A2 density and sensitivity relative to B2 density and sensitivity.

That's a gross generalization, and depends on other factors such as 'genetics', insulin resistance (which can be manipulated with dietary changes), activity level, and thyroid activity (which is affected by all of the above).
 
Since this thread stated ovr 18 months ago, there HAS been human studies showing a direct effect of estrogen on A2 receptors and female fat distribution:

J Clin Endocrinol Metab. 2004 Apr;89(4):1869-78.

Estrogen controls lipolysis by up-regulating alpha2A-adrenergic receptors directly in human adipose tissue through the estrogen receptor alpha. Implications for the female fat distribution.

Pedersen SB, Kristensen K, Hermann PA, Katzenellenbogen JA, Richelsen B.

Department of Endocrinology and Metabolism, Aarhus Amtssygehus, Aarhus University Hospital, Denmark. [email protected]

Estrogen seems to promote and maintain the typical female type of fat distribution that is characterized by accumulation of adipose tissue, especially in the sc fat depot, with only modest accumulation of adipose tissue intraabdominally. However, it is completely unknown how estrogen controls the fat accumulation. We studied the effects of estradiol in vivo and in vitro on human adipose tissue metabolism and found that estradiol directly increases the number of antilipolytic alpha2A-adrenergic receptors in sc adipocytes. The increased number of alpha2A-adrenergic receptors caused an attenuated lipolytic response of epinephrine in sc adipocytes; in contrast, no effect of estrogen on alpha2A-adrenergic receptor mRNA expression was observed in adipocytes from the intraabdominal fat depot. These findings show that estrogen lowers the lipolytic response in sc fat depot by increasing the number of antilipolytic alpha2A-adrenergic receptors, whereas estrogen seems not to affect lipolysis in adipocytes from the intraabdominal fat depot. Using estrogen receptor subtype-specific ligands, we found that this effect of estrogen was caused through the estrogen receptor subtype alpha. These findings demonstrate that estrogen attenuates the lipolytic response through up-regulation of the number of antilipolytic alpha2A-adrenergic receptors only in sc and not in visceral fat depots. Thus, our findings offer an explanation how estrogen maintains the typical female sc fat distribution because estrogen seems to inhibit lipolysis only in sc depots and thereby shifts the assimilation of fat from intraabdominal depots to sc depots.
 
You may also find these interesting.

Tchernof et al. Ovarian Hormone Status and Abdominal Visceral Adipose Tissue Metabolism. J Clin Endocrinol Metab 89: 3425-3420, 2004.

Rodriguez-Cuenca et al. Depot differences in steroid receptor expression in adipose tissue: possible role of the local steroid milieu. Am J Physiol Endocrinol Metab 288: E200-E207, 2005.

Glenmark et al. Difference in skeletal muscle function in males vs. females: role of estrogen receptor-B. Am J Physiol Endocrinol Metab 287: E1125-E1131, 2004.

W6
 
Wilson6/Daisy Girl....not sure how to post PDF files on EF as some of these aren't available (to me) in HTML. If you can tell me how to post PDFs......probably easier to just email Wilson6 or I and have us email you the PDFs. Has the added bonus of not boring everyone else on the board who isn't interested in the nitty-gritty details!
 
MS said:
Wilson6/Daisy Girl....not sure how to post PDF files on EF as some of these aren't available (to me) in HTML. If you can tell me how to post PDFs......probably easier to just email Wilson6 or I and have us email you the PDFs. Has the added bonus of not boring everyone else on the board who isn't interested in the nitty-gritty details!

Yeah, I didn't think you could post PDFs on the board......but I was hoping someone else knew how. :(
 
Even if I knew how to post a PDF, I think there are problems with copyright infringement which I wouldn't want to be involved in by posting in such a public place. Let's stick to emails.
 
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