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Submitted on March 30, 2005
Accepted on June 16, 2005
RELEASE FROM MONONUCLEAR CELLS IN WOMEN WITH POLYCYSTIC OVARY SYNDROME
Dept. of Reproductive Biology, and Dept. of Medicine, Schwartz Center for Metabolism and Nutrition, Case Western Reserve University School of Medicine, Cleveland, OH
* To whom correspondence should be addressed. E-mail: fgonzalez{at}metrohealth.org.
Context: Women with Polycystic Ovary Syndrome (PCOS) are often insulin resistant and have chronic low level inflammation. Objective: The purpose of this study was to determine the effects of hyperglycemia on lipopolysaccaride (LPS)-stimulated TNF
release from mononuclear cells (MNC) in PCOS. Design: A prospective controlled study. Setting: An academic medical center. Patients: Sixteen reproductive age women with PCOS (8 lean, 8 obese) and 14 age-matched controls (8 lean, 6 obese). Main Outcome Measures: Insulin sensitivity (IS) derived from a 2-hour 75 gram oral glucose tolerance test (ISOGTT). Percent truncal fat determined by DEXA. TNF release measured from MNC cultured in the presence of LPS from blood samples drawn fasting and 2 h after glucose ingestion. Results: ISOGTT was lower in women with PCOS compared with controls (3.9 ± 0.4 vs. 6.3 ± 1.0, P < 0.03), and was negatively correlated with % truncal fat (r = 0.56, P < 0.002). Truncal fat was greater in lean women with PCOS compared with lean controls (29.8 ± 2.6 vs. 23.8 ± 2.5%, P < 0.04). The TNF response was different between obese and lean controls (-96.9 ± 21.2 vs. 24.4 ± 21.6 pg/ml, P < 0.03) and obese and lean women with PCOS (-94.1 ± 34.5 vs. 30.4 ± 17.6 pg/ml, P < 0.002). Fasting plasma C-reactive protein was elevated (P < 0.003) in obese PCOS and obese controls compared with lean controls. Conclusion: An increase in abdominal adiposity and increased TNF release from MNC following hyperglycemia may contribute to insulin resistance in lean PCOS. In contrast, obese PCOS have more profound chronic inflammation, and thus may have LPS tolerance which protects them from relatively mild excursions in blood glucose.
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