Journal
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
Volume 86, Issue 9, Pages 4330-4338Publisher
ENDOCRINE SOC
DOI: 10.1210/jc.86.9.4330
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- Medical Research Council [MC_U120061305] Funding Source: researchfish
- Medical Research Council [MC_U120061305] Funding Source: Medline
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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/m(2)]) 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 se 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=0.3-0.6), 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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