Location: Obesity and Metabolism ResearchTitle: In polycystic ovary syndrome, adrenal steroids are regulated differently in the morning versus in response to nutrient intake Author
Submitted to: Fertility and Sterility
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/4/2009
Publication Date: 4/1/2009
Publication URL: http://www.sciencedirect.com/science?_ob=MImg&_imagekey=B6T6K-4VYW6D6-1G-1&_cdi=5033&_user=4421&_pii=S0015028209005366&_origin=search&_coverDate=03%2F01%2F2010&_sk=999069995&view=c&wchp=dGLzVzb-zSkWA&md5=6fccdf4d22f6b20599c51e82c35c57dc&ie=/sdarticle.pdf
Citation: Gurusinghe, D., Gill, S., Almario, R.U., Lee, J., Horn, W.F., Keim, N.L., Kim, K., Kasim-Karakas, S.E. 2009. In polycystic ovary syndrome, adrenal steroids are regulated differently in the morning versus in response to nutrient intake. Fertility and Sterility, 93(4):1192-1193, 2009. Interpretive Summary: Polycystic ovary syndrome (PCOS) is a condition characterized by excess production of male steroid hormones in women, and is often accompanied by bouts of low blood glucose, insulin resistance, and obesity. Other steroid hormones secreted by the adrenal glands are known to influence blood glucose levels, but little is known about how these hormones function in women with PCOS. We found that the steroid hormone response to an oral glucose load was variable in women with PCOS. Those women who had significant increases in cortisol after taking the glucose load had larger swings in blood glucose, a greater insulin response, a greater DHEA response, and were more obese. These women also experienced marked clinical symptoms including shakiness, sweatiness, weakness and hunger, as their cortisol levels increased. These results demonstrate that glucose ingestion causes an increase in adrenal hormones in some women with POCS, which, in turn, produces clinical symptoms that may trigger eating to relieve these symptoms.
Technical Abstract: The objective of this study was to investigate adrenal steroid regulation in Polycystic Ovary Syndrome (PCOS). A 5-h oral glucose tolerance test (OGTT) and a 3-h frequently sampled-intravenous glucose tolerance test (FSIVGTT) were administered to 30 patients with PCOS. Anthropometric parameters (height, weight, body fat) were measured and blood was analyzed for leptin, cortisol, DHEAS, DHEA, glucose and insulin. Morning cortisol correlated with sensitivity index (SI, r = 0.540, p = 0.0109). Morning DHEAS correlated inversely with age (r = -0.6359), body mass index (BMI, r = -0.6199), fat mass (r = -0.630) and leptin (r = -0.5676) (p < 0.002 for all). Between the 2nd and 4th h of OGTT, change in cortisol (') exhibited 3 patterns: I. Responders (n= 9, ': 10.7±1.0 µg/dL), II. Non-responders (n=10, ': -3.5±0.6 µg/dl) and III. Intermediates (n =11, ': 4.3±1.0 µg/dl). As compared to the non-responders, the responders were more obese (BMI: 37.0±1.6 vs. 31.7±1.8 kg/m2, p < 0.05); had higher glucose at 60 min of OGTT (194.6±12.6 vs. 131.1±11.9 mg/dl, p < 0.05), higher area under the curves for glucose (AUCGlucose: 332±20 vs. 265±17 mg/dl, p = 0.0208) and insulin (AUCInsulin: 244±50 vs. 125±30 mU/ml, p = 0.05) and lower nadir glucose (61.4±2.2 vs. 70.2±2.3 mg/dl, p = 0.0002). We conclude that cortisol and DHEAS are regulated differently in the morning vs. in response to nutrient intake. Obesity and insulin resistance are associated with lower morning cortisol and DHEAS but increased cortisol and DHEA responses after glucose ingestion. Therefore, steroid levels measured in the morning may not reflect the day-long steroid exposure.