Because steroids are lipophilic, they diffuse easily through the cell membranes, and therefore have a very large distribution volume. In their target tissues, steroids are concentrated by an uptake mechanism which relies on their binding to intracellular proteins (or " receptors ", see below). High concentration of steroids are also found in adipose tissue, although this is not a target for hormone action. In the human male, adipose tissue contains aromatase activity, and seems to be the main source of androgen-derived estrogens found in the circulation. But most of the peripheral metabolism occurs in the liver and to some extent in the kidneys, which are the major sites of hormone inactivation and elimination, or catabolism (see below).
We have also noted that 24-hour urinary estrogens can be a sensitive monitor of liver detoxification capability. Elevated urinary estrogens in normally-cycling women may indicate a history of exposure to liver stresses such as excessive environmental organic chemicals. Interventions intended to improve liver function result in a gradual normalization of the abnormal estrogen levels. Thus, measurement of urinary estrogens can give insight into other aspects of physiology. This phenomenon is also noted in peri- or post-menopausal women who have previously taken Premarin, and have switched to triple-estrogen replacement with less-than-optimal symptom relief.
Because non-genomic pathways include any mechanism that is not a genomic effect, there are various non-genomic pathways. However, all of these pathways are mediated by some type of steroid hormone receptor found at the plasma membrane.  Ion channels, transporters, G-protein coupled receptors (GPCR), and membrane fluidity have all been shown to be affected by steroid hormones.  Of these, GPCR linked proteins are the most more information on these proteins and pathways, visit the steroid hormone receptor page.