Visceral Fat significant when it comes to PCOS and metabolic syndrome

KatCarney · 03-01-2007, 04:21 PM

BJOG. 2006 Oct;113(10):1203-9. Epub 2006 Jun 2.

The central issue? Visceral fat mass is a good marker of insulin resistance and metabolic disturbance in women with polycystic ovary syndrome.

Quote:

Kat Note: Visceral Fat is fat surrounding the interanal organs:
Visceral: Referring to the viscera, the internal organs of the body, specifically those within the chest (as the heart or lungs) or abdomen (as the liver, pancreas or intestines).

Subcutaneous fat is fat under the skin...the stuff you can pinch.

Lord J, Thomas R, Fox B, Acharya U, Wilkin T.

Department of Obstetrics and Gynaecology, Royal Cornwall Hospital, Truro, Cornwall, UK. jonathan.lord@pms.ac.uk

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).

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.

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 beta-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).