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Submitted on March 25, 2004
Accepted on December 29, 2004
University Hospital of North Staffordshire, and School of Medicine, Keele University, Stoke on Trent, Staffordshire ST4 7QB, UK; Dept of Mathematics, Keele University, Stoke-on-Trent
* To whom correspondence should be addressed. E-mail: r.n.clayton{at}keele.ac.uk.
Polycystic ovary syndrome (PCOS) is associated with hyperandrogenaemia, insulin resistance, altered lipid profile and therefore with subsequently increased risk for metabolic complications such as type 2 diabetes and cardiovascular diseases. It has been reported that sisters of probands with PCOS, who themselves had PCOS or hyperandrogenaemia with normal menses, were more insulin resistant than unaffected sisters. We have previously reported that 60% of first degree relatives (premenopausal mothers and sisters) of PCOS probands had polycystic ovaries (PCO) on ultrascan. Sisters with PCO were more likely to have oligomenorrhoea and increased androgen levels than sisters without PCO. The aims of this study were to assess insulin sensitivity status (HOMA, QUICKI, glucose to insulin ratio (G/I) and lipid profiles in probands with PCOS and their sisters with PCO and without PCO on ultrascan. Mixed model hierarchical regression analysis, to accommodate the non-independent nature of the subjects (family relationships), with the three groups together did not show significant differences in insulin sensitivity, calculated as QUICKI, HOMA and G/I for PCOS probands, through sisters with PCO on ultrascan, to sisters without PCO on ultrascan. There was a significant association of measures of insulin sensitivity with BMI. Lipid parameters did not differ between the groups. These data suggest that presence of PCO on ultrasound scan per se does not predispose to reduced insulin sensitivity in sisters of women with PCOS. Since about 20% of premenopausal women in the general population have PCO on ultrascan, and obesity/overweight is becoming more prevalent, it is important that future studies take full account of the contribution made by obesity to risk factors for metabolic/vascular complications.
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