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The central issue? Visceral fat mass is a good marker of insulin resistance and metabolic disturbance in women with polycystic ovary syndrome
Author(s) -
Lord J,
Thomas R,
Fox B,
Acharya U,
Wilkin T
Publication year - 2006
Publication title -
bjog: an international journal of obstetrics and gynaecology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.157
H-Index - 164
eISSN - 1471-0528
pISSN - 1470-0328
DOI - 10.1111/j.1471-0528.2006.00973.x
Subject(s) - insulin resistance , endocrinology , medicine , polycystic ovary , waist , metabolic syndrome , insulin , population , sex hormone binding globulin , body mass index , homeostatic model assessment , hormone , diabetes mellitus , androgen , environmental health
Objective  To establish whether visceral fat mass is the most significant variable correlating with insulin resistance and other metabolic parameters in women with polycystic ovary syndrome (PCOS). Design  Prospective cross‐sectional trial. Setting  Reproductive medicine clinic. Population  Forty women with anovulatory PCOS. Methods  Measurements were taken at recruitment, and analysis was performed to define correlations between the outcome measures and the explanatory variables. Main outcome measures  Visceral and subcutaneous fat by computed tomography scan, insulin resistance, anthropometric measures, markers of the metabolic syndrome and androgens. Results  Strong linear correlation of visceral fat to insulin resistance ( r = 0.68, P < 0.001) was observed. There were also statistically significant correlations with fasting insulin ( r = 0.73, P < 0.001), homeostasis model assessment β‐cell function ( r = 0.50, P = 0.007), triglycerides ( r = 0.45, P = 0.003), high‐density lipoprotein cholesterol ( r =−0.42, P = 0.007), urate ( r = 0.47, P = 0.002), Sex hormone binding globulin ( r =−0.39, P = 0.01) and luteinising hormone ( r =−0.32, P = 0.02). There were no significant correlations of testosterone with fat distribution or metabolic parameters. Insulin resistance showed closest correlation to visceral fat mass ( r = 0.68, P < 0.001), then to waist circumference ( r = 0.62, P < 0.001), with the weakest correlation being waist:hip ratio ( r = 0.36, P = 0.01). The best regression model for predicting insulin resistance is with visceral fat mass and triglycerides as the explanatory variables ( r = 0.72, P < 0.001). Conclusions  Visceral fat is the most significant variable correlating with metabolic dysfunction in women with PCOS. Our data support the hypothesis that visceral fat either causes insulin resistance or is a very early effect of it. It also implies that reducing visceral fat should reduce insulin resistance which may account for the observations that exercise and weight loss appear to be more effective interventions than pharmacological treatments. The best anthropometric measure of insulin resistance is waist circumference.

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