Gastrointestinal hormone secretion in women with polycystic ovary syndrome: an observational study

STUDY QUESTION: Is the secretion of gastrointestinal hormones impaired in patients with polycystic ovary syndrome (PCOS)? SUMMARY ANSWER: Gastrointestinal hormone levels were abnormal in patients with PCOS. WHAT IS KNOWN ALREADY: The hormones glucagon-like peptide-1 (GLP-1) and peptide tyrosine-tyrosine (PYY) are both involved in signaling satiety. Secretion of GLP-1 and PYY in response to nutrients in the small intestine plays an important role in energy metabolism. Most PCOS patients are overweight or obese, which suggests dysregulation of appetite. STUDY DESIGN, SIZE, DURATION: In order to evaluate levels of gastrointestinal hormones in PCOS, a cohort study was undertaken, involving 30 PCOS patients and 29 BMI-matched healthy women recruited from Shanghai Renji Hospital between 1 March 2013 and 30 May 2014. PARTICIPANTS/MATERIALS, SETTING, METHODS: After an overnight fast, all participants underwent an oral glucose tolerance test. Blood was sampled frequently for measurement of blood glucose and plasma insulin, total GLP-1 and PYY concentrations. MAIN RESULTS AND THE ROLE OF CHANCE: Fasting and postprandial insulin levels were significantly higher in patients with PCOS compared with the healthy controls (P < 0.05). Fasting and postprandial GLP-1 (t = 0 and 30 min; mean +/- SEM) were also higher in PCOS group (17.5 +/- 1.07 pM versus 14.1 +/- 1.16 pM, P < 0.05; 29.7 +/- 2.39 pM versus 22.8 +/- 2.09 pM, P < 0.05). However, there were no differences in plasma PYY between patients with PCOS and healthy controls either fasting or postprandially. PYY levels were lower in obese PCOS patients than in lean PCOS patients (P < 0.05). LIMITATIONS, REASONS FOR CAUTION: The study involved a small number of subjects with PCOS, and examined hormone responses to oral glucose rather than a physiological meal. WIDER IMPLICATIONS OF THE FINDINGS: Deficient secretion of GLP-1 and PYY does not contribute to excessive food intake in the pathophysiology of PCOS.