B
Brian C
Member
- Sep 19, 2010
- 24
- 0
I already knew that t3 up-regluated beta recpetors, so that might cancel out the down regulation that has been shown by clenbuterol.
I also already knew that Androgens, such as testosterone, can bind to these beta receptors and signal lipolysis as well.
But, I have only heard of steroids up-regulateing androgen receptors in skeletal muscle...these receptors are in the nucleus of the cell...beta receptors on fat cells are on the membrane of the cell.
But it appears that that steroids up-regulate beta receptors in adipose tissue as well! And because many people run "unnaturally" high amounts of testosterone/androgens when they run clen, that might be one of the reasons why so many people swear by running clen continuously with good results! (all the studies I am aware of that show clen's down-regulation of beta receptors were without use of steriods)
In the previous studies we have shown that testosterone increases lipolytic responsiveness to catecholamines in rat white adipocytes, and that is associated with an up-regulation of beta-adrenergic receptor density. However, the postreceptor events involved in the testosterone induced enhancement of beta-adrenergic receptor activated lipolysis in these cells have not been adequately studied, and were therefore investigated in the present study. Male Sprague Dawley rats were divided into three groups: control, castrated, and castrated treated with testosterone. The beta-adrenergic receptor-mediated cAMP accumulation, measured with RIA after isoproterenol (a beta-adrenergic agonist) stimulation was decreased in castrated rats, and reversed by testosterone treatment, suggesting a testosterone effect at or proximal to adenylate cyclase. However, no differences between the groups were found in abundance of G alpha protein messenger RNAs (G alpha s, G alpha i-1, and G alpha i-2) as analyzed by Northern blot and a solution hybridization RNase protection assay, or in G protein mass measured with a quantitative enzyme-linked immunosorbent assay in fat cell membrane preparation. Lipolysis stimulated by N6-monobutyryl-cAMP was reduced in castrated rats and recovered by testosterone treatment, suggesting that components distal to the adenylate cyclase, i.e. protein kinase A (PKA) and/or hormone sensitive lipase (HSL) also are involved in testosterone regulation of lipolysis. In conclusion, these and previous results suggest that the testosterone-induced increase in lipolytic response to catecholamines in rat white adipocytes is mediated through several events including an increased beta-adrenergic receptor density, probably an increased adenylate cyclase activity and an increased protein kinase A/hormone sensitive lipase activity at the postreceptor level with apparent absence of effect on the expression of G-proteins.
http://www.ncbi.nlm.nih.gov/pubmed/8384992
I also already knew that Androgens, such as testosterone, can bind to these beta receptors and signal lipolysis as well.
But, I have only heard of steroids up-regulateing androgen receptors in skeletal muscle...these receptors are in the nucleus of the cell...beta receptors on fat cells are on the membrane of the cell.
But it appears that that steroids up-regulate beta receptors in adipose tissue as well! And because many people run "unnaturally" high amounts of testosterone/androgens when they run clen, that might be one of the reasons why so many people swear by running clen continuously with good results! (all the studies I am aware of that show clen's down-regulation of beta receptors were without use of steriods)
In the previous studies we have shown that testosterone increases lipolytic responsiveness to catecholamines in rat white adipocytes, and that is associated with an up-regulation of beta-adrenergic receptor density. However, the postreceptor events involved in the testosterone induced enhancement of beta-adrenergic receptor activated lipolysis in these cells have not been adequately studied, and were therefore investigated in the present study. Male Sprague Dawley rats were divided into three groups: control, castrated, and castrated treated with testosterone. The beta-adrenergic receptor-mediated cAMP accumulation, measured with RIA after isoproterenol (a beta-adrenergic agonist) stimulation was decreased in castrated rats, and reversed by testosterone treatment, suggesting a testosterone effect at or proximal to adenylate cyclase. However, no differences between the groups were found in abundance of G alpha protein messenger RNAs (G alpha s, G alpha i-1, and G alpha i-2) as analyzed by Northern blot and a solution hybridization RNase protection assay, or in G protein mass measured with a quantitative enzyme-linked immunosorbent assay in fat cell membrane preparation. Lipolysis stimulated by N6-monobutyryl-cAMP was reduced in castrated rats and recovered by testosterone treatment, suggesting that components distal to the adenylate cyclase, i.e. protein kinase A (PKA) and/or hormone sensitive lipase (HSL) also are involved in testosterone regulation of lipolysis. In conclusion, these and previous results suggest that the testosterone-induced increase in lipolytic response to catecholamines in rat white adipocytes is mediated through several events including an increased beta-adrenergic receptor density, probably an increased adenylate cyclase activity and an increased protein kinase A/hormone sensitive lipase activity at the postreceptor level with apparent absence of effect on the expression of G-proteins.
http://www.ncbi.nlm.nih.gov/pubmed/8384992