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Lean mass and insulin resistance in women with polycystic ovary syndrome
Abstract Insulin resistance is common in women with polycystic ovary syndrome (PCOS). Muscle is the major tissue utilizing glucose while excess adipose tissue relates to insulin resistance. Thus, body composition is likely to be an important regulator of insulin sensitivity. Thirty-nine PCOS patient...
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Published in: | Metabolism, clinical and experimental clinical and experimental, 2012-09, Vol.61 (9), p.1256-1260 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Abstract Insulin resistance is common in women with polycystic ovary syndrome (PCOS). Muscle is the major tissue utilizing glucose while excess adipose tissue relates to insulin resistance. Thus, body composition is likely to be an important regulator of insulin sensitivity. Thirty-nine PCOS patients (age: 29.9 ± 1.0 years; BMI: 33.8 ± 1.2 kg/m2 ) participated in a cross sectional study. Body composition was measured by dual energy x-ray absorptiometry (DEXA). Insulin resistance and secretion were assessed using oral glucose tolerance test (OGTT) and frequently sampled intravenous glucose tolerance test (FS-IVGTT). In contrast with the conventional expectations, lean mass correlated directly ( P < .05) with the insulin resistance measure HOMA ( r = 0.440); and inversely with the insulin sensitivity index QUICKI ( r = −0.522) independent of fat mass. In 11 pairs of subjects matched for fat mass (35.6 ± 2.2 and 35.6 ± 2.4 kg) but with discordant lean mass (52.8 ± 1.8 vs 44.4 ± 1.6 kg), those with higher lean mass had a higher glucose response during OGTT (AUCGlucose ; P = .034). In contrast, 17 pairs matched for lean mass (48.7 ± 1.7 and 48.9 ± 1.6 kg) but discordant for fat mass (43.3 ± 2.6 vs 30.3 ± 8.9 kg) showed no differences in insulin resistance parameters. These novel findings indicate that lean mass relates directly to insulin resistance in PCOS. |
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ISSN: | 0026-0495 1532-8600 |
DOI: | 10.1016/j.metabol.2012.02.004 |