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Insulin resistance higher among women with PCOS
No relationship found with fat distribution among women with PCOS and controls.
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Data from a recent cross-sectional study revealed no significant difference between fat depot measurements of obese women with polycystic ovary syndrome and matched controls.
Researchers in England set out to determine whether obesity-related predisposition to PCOS could reflect overall adiposity. They compared cross-sectional distributions of visceral, abdominal and gluteofemoral adipose tissue in 22 BMI and fat mass-matched pairs of women with PCOS and controls. They also conducted a whole-group comparison of 50 women with PCOS and 28 control women.
The distribution of visceral, abdominal and gluteofemoral fat depots was indistinguishable between women with PCOS and BMI and women in the group who were fat-massed matched, according to the researchers (visceral, P=.40; abdominal, P=.22; gluteal, P=.67; midfemoral, P=.37).
The findings were published in the Journal of Clinical Endocrinology & Metabolism. The whole-group comparison showed no difference even after the researchers adjusted for age and fat mass.
However, insulin concentrations and insulin sensitivity were significantly higher among women with PCOS compared with controls. Excessive insulin resistance in PCOS appears to be independent of visceral adiposity, according to the researchers.
“These data suggest that the characteristic metabolic abnormalities of PCOS are not as closely linked to increased abdominal adiposity as has previously been proposed,” the researchers wrote.
The researchers of this exciting cross-sectional study set out to compare the distribution of visceral fat and adipose tissue in women with PCOS and a control group using a novel technique of axial magnetic resonance imaging scans. Fifty women with PCOS were compared with 28 control women. No difference was found in the distribution of fat within the visceral and adipose tissue between matched pairs of PCOS cases and controls. However, the researchers did find significantly higher fasting serum insulin concentrations and homeostasis model assessment 2-insulin resistance in the PCOS group; the PCOS group was more insulin resistant.
These new findings demonstrate that the driving force behind the changes in PCOS is hyperinsulinemia and not the fat content. The methodology is interesting; the definition of PCOS encompasses the wide spectrum of the phenotype of the disease, which could weaken their findings. However, the MRI scanning of fat distribution is faultless. The researchers admirably highlighted their own limitations in the report, allowing us to look beyond these weaknesses and reflect on the findings. Their purist approach to match BMI and fat mass between the groups reduced their sample size to 22 matched pairs. The ages of the groups were unable to be matched; however, we agree with the researchers that this is a confounding variable.
Elegantly in a small sample the researchers have shown that the insulin resistance in PCOS is independent of visceral adiposity. We believe these findings bring us one step closer in unraveling the mechanism behind the metabolic abnormalities of PCOS, opening new doors for therapeutic intervention and prevention.
– Anita Banerjee, MD
Endocrine fellow, Hammersmith Hospital, London
– Lois Jovanovic, MD
CEO and Chief Scientific Officer, Sansum Diabetes Research Institute, Santa Barbara, Calif.
For more information:
- Barber TM, Golding SJ, Alvey C, et al. Global adiposity rather than abnormal regional fat distribution characterizes women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2008;93:999-1004.