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.
Utilization of these drugs is common in patients with HF. In a study from Denmark, 34 percent of patients received at least one nonsteroid anti-inflammatory agent or cyclooxygenase-2 inhibitor after discharge for first hospitalization for HF [ 2 ]. Use of some of these drugs may be increasing. As an example, a review of Medicare beneficiaries hospitalized with the diagnoses of HF and diabetes mellitus found that the proportion using metformin and/or a thiazolidinedione increased from percent in 1998 to 1999 to percent in 2000 to 2001 [ 3 ].
Diabetes results from inadequate levels of insulin. Type I diabetes is characterized by inadequate levels of insulin secretion, often due to a genetic cause. Type II usually develops in adults from both genetic and environmental causes. Loss of response of targets to insulin rather than lack of insulin causes this type of diabetes. Diabetes causes impairment in the functioning of the eyes, circulatory system, nervous system, and failure of the kidneys. Diabetes is the second leading cause of blindness in the US. Treatments involve daily injections of insulin, monitoring of blood glucose levels and a controlled diet.