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Relation of nutrients and hormones in polycystic ovary syndrome.
Am J Clin Nutr. 2007 Mar; 85(3):688-94.AJ

Abstract

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).

DESIGN

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.

Authors+Show Affiliations

Department of Internal Medicine, Division of Endocrinology, Clinical Nutrition and Vascular Medicine, University of California, Davis, CA 95817, USA. sekarakas@ucdavis.eduNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17344488

Citation

Kasim-Karakas, Sidika E., et al. "Relation of Nutrients and Hormones in Polycystic Ovary Syndrome." The American Journal of Clinical Nutrition, vol. 85, no. 3, 2007, pp. 688-94.
Kasim-Karakas SE, Cunningham WM, Tsodikov A. Relation of nutrients and hormones in polycystic ovary syndrome. Am J Clin Nutr. 2007;85(3):688-94.
Kasim-Karakas, S. E., Cunningham, W. M., & Tsodikov, A. (2007). Relation of nutrients and hormones in polycystic ovary syndrome. The American Journal of Clinical Nutrition, 85(3), 688-94.
Kasim-Karakas SE, Cunningham WM, Tsodikov A. Relation of Nutrients and Hormones in Polycystic Ovary Syndrome. Am J Clin Nutr. 2007;85(3):688-94. PubMed PMID: 17344488.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Relation of nutrients and hormones in polycystic ovary syndrome. AU - Kasim-Karakas,Sidika E, AU - Cunningham,Wendy M, AU - Tsodikov,Alex, PY - 2007/3/9/pubmed PY - 2007/4/27/medline PY - 2007/3/9/entrez SP - 688 EP - 94 JF - The American journal of clinical nutrition JO - Am. J. Clin. Nutr. VL - 85 IS - 3 N2 - 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). DESIGN: 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. SN - 0002-9165 UR - https://www.unboundmedicine.com/medline/citation/17344488/Relation_of_nutrients_and_hormones_in_polycystic_ovary_syndrome_ L2 - https://academic.oup.com/ajcn/article-lookup/doi/10.1093/ajcn/85.3.688 DB - PRIME DP - Unbound Medicine ER -