Need a Reference on estrogen & A2 receptors

[MS]

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:testrogesterone: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.

 

[macrophage69alpha]

damn xenoestrogens

 

[fawnmarie]

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

 

[MS]

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

 

[fawnmarie]

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

 

[MS]

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).

 

[Daisy_Girl]

ANother bump - good info to help understand estrogen and our bodies.

 

[MS]

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.

 

[Daisy_Girl]

Thanks MS - I miss all your studies.

 

[wilson6]

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