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Other Original Articles |
Endocrine Unit (A.P.G., J.K.H., S.R.B.); MRI Unit (E.L.T., J.D.B., N.S., J.V.H.), MRC Clinical Sciences Centre; Department of Dietetics (A.E.B., G.F.), Imperial College School of Medicine, Hammersmith Hospital, London W12 0NN, United Kingdom; and Section of Developmental Psychiatry (A.H.), University of Cambridge CB2 2AH, United Kingdom
Address all correspondence and requests for reprints to: Prof. S. R. Bloom, Department of Metabolic Medicine, 6th Floor Commonwealth Building, Imperial College School of Medicine, Hammersmith Campus, Du Cane Road, London W12 0NN, United Kingdom.
Abstract
Visceral obesity is detrimental to health, but the mechanisms controlling body fat distribution are not fully understood. In premenopausal adult females (30 nonobese, 14 obese [body mass index >30kg/m2]), variance in fasting insulin, glucose, insulin/glucose ratio, C-peptide/insulin ratio, triglycerides, and high-density lipoprotein/low-density lipoprotein-cholesterol ratio, were independently influenced by visceral but not total sc or abdominal sc adipose tissue, as measured by whole-body magnetic resonance imaging. Adult females with Prader-Willi syndrome (n = 13) had significantly reduced visceral adiposity, compared with obese controls (visceral/total sc adipose tissue ratio: 0.067 ± 0.017 vs. 0.108 ± 0.021), independent of their total adiposity (P < 0.001), or use of exogenous sex steroids. This is in contrast to that expected by their physical inactivity, hypogonadism, adult GH deficiency, and psychiatric problems. Females with Prader-Willi syndrome not receiving sex steroids (n = 8) had significantly reduced fasting insulin, insulin/glucose ratio, and triglycerides and increased C-peptide/insulin ratio, compared with obese controls, adjusting for total (P < 0.05) but not visceral adiposity (P = 0.30.6), supporting their association. The cause of the reduced visceral adiposity in Prader-Willi syndrome may reflect novel hormonal, hypothalamic, and/or genetic influences on body fat distribution.
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