A study and soem questions
Department of Obstetrics-Gynecology and Biochemistry, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-9032, USA.
Anabolic steroids are synthetic derivatives of testosterone and are characterized by their ability to cause nitrogen retention and positive protein metabolism, thereby leading to increased protein synthesis and muscle mass. There are disagreements in the literature in regards to the interaction of anabolic steroids with the androgen receptor (AR) as revealed by competitive ligand binding assays in vitro using cytosolic preparations from prostate and skeletal muscle. By use of tissue extracts, it has been shown that some anabolic steroids have binding affinities for the AR that are higher than that of the natural androgen testosterone, while others such as stanozolol and methanedienone have significantly lower affinities as compared with testosterone. In this study we show that stanozolol and methanedienone are low affinity ligands of the rat recombinant AR as revealed by a ligand binding assay in vitro, however, based on a cell-based AR-dependent transactivation assay, they are potent activators of the AR. We also show that a single injection of stanozolol and methanedienone causes a rapid cytosolic depletion of AR in rat skeletal muscle. Based on these results, we conclude that anabolic steroids with low affinity to AR in vitro, can in fact in vivo act on the AR to cause biological responses.
PMID: 15876413 [PubMed - indexed for MEDLINE]
Now those 2 steroids obviously have been proven to not cause muscle loss, which is what I am getting from the bold sentence basically, assuming a reduction of ARs in skeletal muscle is exactly the opposite of what we are all trying to do, but how does a steroid work by activating the receptor as opposed to binding to it if the result is a decrease in ARs ? Does "activating" the AR cause an increase in sensitivity to steroids? I mean what is the differnce between activating and binding ?
