Polycystic ovary syndrome (PCOS) is a common and complex endocrine disorder,
often accompanied and complicated by insulin resistance, glucose intolerance and obesity.
Gut, brain and metabolism are highly related with each other in obesity and diabetes as well
as in PCOS. Central nervous system regulates food intake through complex interactions of
homeostatic and hedonic systems while gastrointestinal system contributes to food intake
and metabolism via orexigenic and anorexigenic gastrointestinal hormones. Ghrelin is the
only circulating orexigenic hormone whereas anorexigenic peptides include glucagon like
peptide-1 (GLP-1), gastric inhibitory peptide (GIP), peptide YY (PYY) and cholecystokinin
(CCK). Compared to healthy women, patients with PCOS show decreased or unaltered fasting
ghrelin levels, along with decreased or unaltered postprandial suppression of this hormone.
GLP-1, PYY and CCK show unaltered or decreased levels both in fasting and postprandial
states in PCOS whereas fasting levels of another gut hormone, GIP is either unaltered
or increased. Dietary interventions associated with weight loss or short term oral contraceptive use in PCOS
do not alter fasting or postprandial levels of these hormones. However use of metformin is associated with an
increase in ghrelin, PYY, GLP-1 and GIP in women with PCOS. GLP-1 agonists and bariatric surgery, both having
a significant impact on gut-brain axis, appear to be effective therapeutic options in obese women with PCOS.
Finally, alterations in gut microbiota and possible interactions with gut-brain axis in PCOS is a topic of interest.
Understanding the relationship between PCOS and homeostatic and hedonic systems, gastrointestinal hormones,
and gut microbiota as well as potential effects of different therapeutic interventions on these systems will provide
further understanding and novel treatment opportunities for this syndrome.
Keywords: Polycystic ovary syndrome, ghrelin, GLP-1, GIP, PYY, CCK, appetite, microbiota.
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