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.
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, dehydroepiandrosterone (DHEA) and androstenedione. Thus, fasciculata and reticularis cells can make corticosteroids and the adrenal androgens, but not aldosterone.
Removal of the parathyroid glands in mammals causes a fall in the level of calcium in the blood plasma, which, if sufficiently severe, is accompanied by convulsions and other symptoms resulting from increased excitability of the motor nerves. These symptoms can be corrected by injection of appropriate preparations of parathyroid glands. The activity of the glands, like that of the ultimobranchial tissue, is regulated by negative feedback; ., lowering of the plasma calcium level increases the output of parathormone (but decreases the output of calcitonin). The hypercalcemic effect (., increase in level of blood calcium) of the hormone depends largely upon its action on bone, since it promotes the transfer of calcium from this tissue into the plasma, probably by a direct action on the active bone-forming cells ( osteocytes ). In addition, however, parathormone promotes the formation of new bone tissue, and thus also increases its metabolic activity and the turnover of its structural material. Other effects of parathormone, at least in part, contribute to the elevation of plasma calcium; ., PTH increases both the absorption of calcium by the intestine and its resorption by the kidney tubule. Since, however, the hypercalcemia induced by the hormone results in more of it passing into the kidney tubule, the net result may be increased excretion of calcium despite the increased resorption. Other actions of the hormone, less easy to relate to its well-defined influence upon calcium metabolism, include a regulatory influence upon the level of magnesium in blood plasma and upon the rate of removal of phosphate from urine.