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.
Boys with too little androstenedione may fail to develop the sexual characteristics associated with puberty, including pubic and body hair, growth of the sexual organs and deepening of the voice. Similarly, girls may fail to start their periods and may not undergo many of the changes usually seen in puberty. In addition, if a male foetus has too little androstenedione, he may be born with abnormal genitalia. Too little androstenedione in later life would cause the same changes for both men and women as too little testosterone and oestrogen.