Insulin resistance has been described as associated with low levels of mannan-binding lectin (MBL), a protein of the innate immune system (1). The aim of the present study was to study serum MBL concentration in polycystic ovary syndrome (PCOS) in relation to insulin resistance, adiponectin, and high-sensitivity C-reactive protein (hsCRP). Insulin sensitivity, serum MBL concentration, adiponectin, hsCRP, and sex hormones were measured in 102 PCOS (34 of whom were lean and 68 overweight or obese) and 50 healthy (28 lean and 22 overweight or obese) women. The diagnosis of PCOS was done according to Rotterdam Consensus Criteria. In the factorial ANOVA, we observed that both PCOS (P < 0.001) and obesity (P = 0.034) independently contributed to lower serum MBL (in those with obese PCOS, 1,786.92 ± 1,747.02; lean PCOS, 2,304.68 ± 2,137.35; obese control, 2,969.88 ± 2,615.97; and lean control, 4,007.87 ± 2,132.62 μg/l; P = 0.54 for the interaction) and lower insulin sensitivity (obese PCOS, 7.20 ± 3.29; lean PCOS, 9.52 ± 3.75; obese control, 9.05 ± 3.16; and lean control, 11.38 ± 3.07 mg · kgfat-free mass −1 · min−1 [PCOS, P = 0.002; obesity, P < 0.001; P = 0.99 for the interaction]). Serum adiponectin was lower (P < 0.001) and hsCRP was higher (P = 0.0011) in the obese women, whereas PCOS had no effect.
Serum MBL level was positively related to insulin sensitivity (r = 0.29, P = 0.00025). This relationship persisted after controlling for age, BMI, waist circumference, serum cholesterol, fasting triglycerides, HDL cholesterol, and adiponectin (all adjusted β-values between 0.19 and 0.29, all P < 0.01). Serum MBL was also negatively associated with hsCRP (r = −0.24, P = 0.006). We did not find any association between MBL and markers of hyperandrogenism, suggesting that low MBL is connected with insulin resistance and proinflammatory activity rather than with PCOS per se. We demonstrated that in PCOS women, decreased MBL levels might contribute to insulin resistance and thus to an increased risk of type 2 diabetes and cardiovascular disease.
This study was supported by grant 3 P05A 002 25 from Poland's Ministry of Science and Higher Education (Warsaw, Poland), grant 3-50741L from Medical University of Bialystok (Bialystok, Poland), and CIBER Fisiopatologia de la Obesidad y Nutricion CB/06/03/010 (Girona, Spain).