Cortisol and the polycystic ovary syndrome

Abstract

Adrenal steroidogenesis is under the control of the hypothalamic–pituitary–adrenal (HPA) axis. Furthermore, metabolic factors including insulin and obesity-related signals may play a role in the regulation of both enzymes involved in the steroidogenetic pathways, as well as in the regulation of the HPA axis. In women with the polycystic ovary syndrome (PCOS), cortisol production rate is probably normal, although adrenal androgens can be overproduced in a subset of affected women. Cortisol metabolism and regeneration from inactive glucocorticoids can also be disrupted in PCOS, thereby contributing to determining an adrenal hyperandrogenic state. Finally, overactivity of the HPA axis may be related to the high prevalence of psychopathological and eating disorders in women with PCOS, implying a maladaptive allostatic load in the adaptive mechanisms to chronic stress exposure.

Keywords::

• 11β-hydroxysteroid dehydrogenase type 1
• cortisol
• eating behavior
• hypothalamic–pituitary–adrenal axis
• insulin
• obesity
• polycystic ovary syndrome
• stress

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.