Estrogen and a2 adrenergic receptor expression
- 02-14-2008, 05:19 PM
Estrogen and a2 adrenergic receptor expression
This paper is a few years old, so forgive me if this has been discussed before. I searched and couldn't find a thread similar to this.
This article shows that estrogen upregulates the anti-lipolytic a2 adrenergic receptor (the one everyone tries to block with ). If you take what they say here, combined with what we know about subQ fat and aromatase expression, it seems as though using an AI either topical (formastane?) or systemically might be a good addition to a topical cycle for fat loss.
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@example.com
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.
- 02-20-2008, 12:58 PM
- 02-20-2008, 03:59 PM
I'm not sure. I have some Rebound XT that I was going to give a try. Maybe topical like Formastane would be a good option as well.
02-20-2008, 04:39 PM
02-20-2008, 05:24 PM
03-18-2008, 06:57 PM
do you think that 3,3'-diindolylmethane would work as a estrogen blocker? I know it does not block estrogen,but changes it to a better estrogen. I wonder if it would be a alternitve?
03-24-2008, 06:11 PM
Well, I know Indole 3 carbinol can inhibit E2 receptor expression and function, but I think it might also affect androgen receptor function as well. It might be a better bet going with something like ATD or formastane since they are a little better defined as far as activity goes.
04-02-2008, 11:05 PM
Try Some Extra Strength Chrysin Itsa Flavone Which It Should Scifit Have One Which Isnt To Expensive I Usually Take These While Im On Test Boosters !
08-02-2008, 06:35 PM
Great study find.
Would cortisol blockers work as well? I have always wondered if cortisol blocking fatburners have more of an effect on subq fat than we realize or if it SOLELY works on visceral.
08-08-2008, 11:20 AM
08-08-2008, 01:23 PM
I've also wondered (and have mentioned this on another thread) since estrogen increases the number of A2 receptors in Subq adipose tissue, is there anything pharmaceutical or otc supplemental that would DECREASE the number of A2 receptors. I know yohimbine hcl acts as an ANTAGONIST, but as far as I know, it doesn't work to reduce the number of A2's. (IE like the new drug faslodex reduces estrogen receptors).
Not that we want to eliminate ALL of our A2 receptors. They are essential for certain human functions and health but an over abundance isn't necessarily good either.
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