Relation of nutrients and hormones in polycystic ovary syndrome.
BACKGROUND
Insulin resistance, infertility, and hirsutism, common characteristics of polycystic ovary syndrome (PCOS), improve with even modest weight loss. Optimal dietary treatment for PCOS is not known.


OBJECTIVE
We compared the effects of acute protein administration with those of glucose challenges on hormones related to obesity and insulin resistance (ie, cortisol and insulin), hirsutism [ie, dehydroepiandosterone (DHEA) and androstenedione], and hunger (ie, ghrelin).


METHODS
Patients with PCOS (n = 28; aged 26 +/- 2 y) were tested with a 5-h oral-glucose-tolerance test (OGTT) and a euvolemic, euenergetic protein challenge.


RESULTS
Glucose ingestion caused larger fluctuations in blood glucose and more hyperinsulinemia than did protein (P < 0.01, overall treatment-by-time interaction). During the protein challenge, cortisol and DHEA declined over 5 h. During OGTT, cortisol and DHEA increased after the third hour and began to show significant divergence from protein from the fourth hour (P <or= 0.01). During OGTT, 18 patients who had a blood glucose nadir of <69 mg/dL had elevated cortisol (baseline: 10.4 +/- 0.4; nadir: 5.9 +/- 0.1; peak: 12.7 +/- 0.9 microg/dL) and DHEA (baseline: 15.6 +/- 1.3; nadir: 11.2 +/- 1.0; peak: 24.6 +/- 1.6 ng/mL) (P < 0.01), whereas the remaining 10 patients with a glucose nadir of 76 +/- 2 mg/dL had no increase in adrenal steroids. Both glucose and protein suppressed ghrelin (from 935 +/- 57 to 777 +/- 51 pg/mL and from 948 +/- 60 to 816 +/- 61 pg/mL, respectively). After glucose ingestion, ghrelin returned to baseline by 4 h and increased to 1094 +/- 135 pg/mL at 5 h. After the protein challenge, ghrelin remained below the baseline (872 +/- 60 pg/mL) even at 5 h. The overall treatment effect was highly significant (P < 0.0001).


CONCLUSIONS
Glucose ingestion caused significantly more hyperinsulinemia than did protein, and it stimulated cortisol and DHEA. Protein intake suppressed ghrelin significantly longer than did glucose, which suggested a prolonged satietogenic effect. These findings provide mechanistic support for increasing protein intake and restricting the simple sugar intake in a PCOS diet.
Kasim-Karakas
Sidika E
SE
Department of Internal Medicine, Division of Endocrinology, Clinical Nutrition and Vascular Medicine, University of California, Davis, CA 95817, USA. sekarakas@ucdavis.edu
Cunningham
Wendy M
WM
Tsodikov
Alex
A
D000328:Adult; D000735:Androstenedione / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism*; D015992:Body Mass Index; D003687:Dehydroepiandrosterone / Q000097:blood; D005260:Female; D005502:Food; D054439:Ghrelin; D005951:Glucose Tolerance Test; D006728:Hormones / Q000097:blood*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007328:Insulin / Q000097:blood; D007700:Kinetics; D008875:Middle Aged; D036361:Peptide Hormones / Q000097:blood; D011085:Polycystic Ovary Syndrome / Q000097:blood*
D001786:Blood Glucose; D054439:Ghrelin; D006728:Hormones; D007328:Insulin; D036361:Peptide Hormones; D000735:Androstenedione; D003687:Dehydroepiandrosterone; D006854:Hydrocortisone