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Obesity (Silver Spring). 2011 Feb;19(2):269-75. doi: 10.1038/oby.2010.274. Epub 2010 Dec 2.

Insulin sensitivity and regional fat gain in response to overfeeding.

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1
Endocrine Research Unit, Mayo Clinic, Rochester, Minnesota, USA.

Abstract

Although insulin resistance and type 2 diabetes (T2DM) are associated with upper body fat distribution, it is unknown whether insulin resistance predisposes to upper body fat gain or whether upper body fat gain causes insulin resistance. Our objective was to determine whether insulin sensitivity predicts abdominal (subcutaneous and/or visceral) fat gain in normal weight adults. Twenty-eight (15 men) lean (BMI = 22.1 ± 2.5 kg/m(2)), healthy adults underwent ~8 weeks of overfeeding to gain ~4 kg fat. Body composition was assessed before and after overfeeding, using dual-energy X-ray absorptiometry (DXA) and abdominal computed tomography to measure total and regional (visceral, abdominal, and lower body subcutaneous) fat gain. We assessed insulin sensitivity with an intravenous glucose tolerance test (IVGTT) and the 24-h insulin area under the curve (AUC). We found a wide range of insulin sensitivity and a relatively narrow range of body fat distribution in this normal weight cohort. Participants gained 3.8 ± 1.7 kg of body fat (4.6 ± 2.2 kg body weight). The baseline 24-h AUC of insulin concentration was positively correlated with percent body fat (r = 0.43, P < 0.05). The contribution of leg fat gain to total fat gain ranged from 29 to 79%, whereas the contributions of abdominal subcutaneous fat and visceral fat gain to total fat gain ranged from 17 to 69% and -5 to 22%, respectively. Baseline insulin sensitivity, whether measured by an IVGTT (S(i)) or the 24-h AUC insulin, did not predict upper body subcutaneous or visceral fat gain in response to overfeeding. We conclude that reduced insulin sensitivity is not an obligate precursor to upper body fat gain.

PMID:
21127472
PMCID:
PMC3711092
DOI:
10.1038/oby.2010.274
[Indexed for MEDLINE]
Free PMC Article
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