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Submitted on October 24, 2005
Accepted on January 26, 2006
B TRIGGERS INFLAMMATION AND INSULIN RESISTANCE IN 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 44109
* To whom correspondence should be addressed. E-mail: fgonzalez{at}metrohealth.org.
Context: Insulin resistance and chronic low level inflammation are often present in women with Polycystic Ovary Syndrome (PCOS). Objective: The purpose of this study was to determine the effects of hyperglycemia on nuclear factor kB (NFkB) activation and inhibitory kB (IkB) 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 16 age- and body composition-matched controls (8 lean, 8 obese). Main Outcome Measures: Insulin sensitivity (IS) was derived from a 2-hour 75 gram oral glucose tolerance test (ISOGTT). Intranuclear NFkB and IkB protein expression were quantitated from MNC obtained from blood drawn fasting and 2 h after glucose ingestion. Results: ISOGTT was lower in PCOS compared with controls (3.3 ± 0.3 vs. 6.4 ± 0.9, P < 0.004). The % change in intranuclear NFkB from mononuclear cells (MNC) was higher in lean and obese PCOS compared with lean controls (42.5 ± 19.1 and 54.5 ± 12.5 vs. -14.1 ± 10.9, P < 0.006). The % change in intranuclear NFkB from MNC correlated positively with 2 h post glucose ingestion levels (r=0.37, P < 0.04) and plasma testosterone (r=0.49, P < 0.006), and correlated negatively with ISOGTT (r=0.39, P < 0.04). The % change in IkB from MNC was lower in lean and obese PCOS compared with lean controls (-22.32 ± 3.2 and -17.0 ± 5.0 vs. 8.4 ± 11.8, P < 0.02). Conclusion: In response to hyperglycemia, intranuclear NFkB increases and IkB decreases in MNC of women with PCOS independent of obesity. This may represent a cardinal inflammatory signal that contributes to the induction of insulin resistance and hyperandrogenism in PCOS.
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