Body fat and insulin resistance independently predict increased serum C-reactive protein in hyperandrogenic women with polycystic ovary syndrome

Abstract

Objective: Increased serum C-reactive protein (CRP), an independent predictor of coronary heart disease, was reported in women with polycystic ovary syndrome (PCOS). It remains unclear whether this finding is due to the association between PCOS and either insulin resistance, obesity, or androgen excess, which are all common features of this condition. The aims of this study were to assess whether increased serum CRP is a specific feature of PCOS and to investigate the mechanisms underlying this association. Design and methods: Serum high-sensitivity CRP (hs-CRP) was measured in 86 hyperandrogenic women (age 21.6G4.2 years, body mass index (BMI) 23.6G3.5 kg/m 2 ), 50 with PCOS and 36 with idiopathic hyperandrogenism (HA). Thirty-five BMI-matched healthy women were also studied as controls. In these subjects, endocrine and metabolic profiles were assessed. In all hyperandrogenic subjects and 14 controls, insulin sensitivity was measured by the glucose clamp technique. Body fat was measured by bioelectrical impedance. Results: Hs-CRP concentrations were higher in PCOS women (3.43G2.01 mg/l) than in HA subjects and healthy women (2.43G1.04, P!0.005; and 2.75G0.86 mg/l, P!0.05 respectively versus PCOS). In multiple regression analyses, increased serum hs-CRP was independently predicted by higher body fat and lower insulin sensitivity. However, in lean women, serum-free testosterone was an additional, negative, predictive variable. Conclusions: PCOS is accompanied by a low-grade chronic inflammation. Body fat appears the main determining factor of this finding, which is only partly explained by insulin resistance. At least in lean women, androgen excess per se seems to play an additional, possibly protective, role in this association.

The polycystic ovary syndrome (pcos) status and cardiovascular risk in young women

“…Additionally, similar to Puder et al' and Shroff et al' findings [35,42], we noted that total fat mass in particular reduced the BMI-related contribution to hsCRP variability the most, suggesting that at least part of the observed association of BMI and hsCRP in PCOS may have been driven by total fat mass. With similar results to our own, a very recent study by Tosi et al noted a negative correlation between TT and hsCRP levels in the studied population (controls, PCOS women, and women with idiopathic hyperandrogenism) [44]. In PCOS subjects, either no correlation [11,42,45] or a positive association between increased androgen levels and indices of chronic inflammation [10,39] were described.…”

“…The increased body adiposity found in both the PCOS group and control group is most likely the explanation for the elevated levels of hsCRP that were found in our control group, as well. It should be also mentioned that in all the studies which have noted higher levels of hsCRP in PCOS women compared with controls, the subjects either were not matched for trunk fat mass as evaluated by DXA or abdominal CT [37,[42][43][44], or if they were matched for BMI, the PCOS women might have had a higher proportion of visceral fat, since they did not carry out direct measurements of fat and lean body mass by scanning [15,45]. Furthermore, hsCRP was significantly and positively correlated with variables of obesity and insulin resistance, and CT, and negatively correlated with TT in PCOS, suggesting that obesity and metabolic alterations, rather than hyperandrogenemia, have a negative impact on markers of chronic inflammation in PCOS subjects.…”

Evaluation of Oxidative Stress and hsCRP in Polycystic Ovarian Syndrome in a Tertiary Care Hospital

“…It was seen that out of the total 116 patients, 46.5 % patients had hsCRP levels [3 mg/l. Tosi et al [33] hypothesised that adiposity was a main factor determining elevated CRP in PCOS patients.…”

Metabolic Aspects of Polycystic Ovary Syndrome

“…Furthermore, insulin resistance in PCOS patients is closely associated with abdominal obesity and hyperandrogenism [60][61][62][63], and PCOS patients are generally insulin resistant at lower BMI levels (27-28 kg/m 2 ) than healthy controls [9, 58,64,65]. However, heterogeneity within the PCOS sample is reflected by more conflicting results regarding insulin resistance in lean PCOS patients with some studies [61,[66][67][68][69] indicating increased insulin resistance and other [70][71][72][73] indicating no difference between lean PCOS patients and weightmatched controls. In some studies [74,75] PCOS patients without hyperandrogenic features are not insulin resistant.…”