Steroid hormones exert their action on target cells by binding to

Genetic conditions, such as Klinefelter’s syndrome and Turner syndrome , can also result in high luteinising hormone levels. Klinefelter’s syndrome is a male-only disorder and results from carrying an extra X chromosome (so that men have XXY, rather than XY chromosomes). As a result of this, the testes are small and do not secrete adequate levels of testosterone to support sperm production. Turner syndrome is a female-only disorder caused by a partial or full deletion of an X chromosome (so that women have XO, rather than XX). In affected patients, ovarian function is impaired and therefore luteinising hormone production increases to stimulate ovarian function.  

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.

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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.

Steroid hormones exert their action on target cells by binding to

steroid hormones exert their action on target cells by binding to

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.

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