Sex hormone-binding globulin (SHBG) is thought to mainly function as a transporter and reservoir for the estradiol and testosterone sex hormones. However it has also been demonstrated that SHBG can bind to a cell surface receptor (SHBG-R). The SHBG-R has not been completely characterized. A subset of steroids are able to bind to the SHBG/SHBG-R complex resulting in an activation of adenylyl cyclase and synthesis of the cAMP second messenger.  Hence the SHBG/SHBG-R complex appears to act as a transmembrane steroid receptor that is capable of transmitting signals to the interior of cells.
Each user experiences their own unique feelings when using steroids and coming off the drug. When someone chooses to stop using they can experience a variety of withdrawal symptoms linked to addiction. Symptoms can include mood swings, fatigue, restlessness, loss of appetite, insomnia, reduced sex drive, the desire to take more steroids, and depression. Evidence for steroid addiction is certainly not as strong as it is for other drugs like cocaine or heroin. Though it is clear that people develop a tolerance and dependence on them and willingly experience negative consequences when using steroids - both of which are signs for drug dependence.
Cells of the zona fasciculata and zona reticularis lack aldosterone synthase (CYP11B2) that converts corticosterone to aldosterone, and thus these tissues produce only the weak mineralocorticoid corticosterone. However, both these zones do contain the CYP17A1 missing in zona glomerulosa and thus produce the major glucocorticoid, cortisol. Zona fasciculata and zona reticularis cells also contain CYP17A1, whose 17,20-lyase activity is responsible for producing the androgens, dehydroepiandosterone (DHEA) and androstenedione. Thus, fasciculata and reticularis cells can make corticosteroids and the adrenal androgens, but not aldosterone.