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1 From the New York Obesity Research Center (DG, J-EY, JA, FXP-S, and SH) and the Department of Radiology (LB), St Luke's–Roosevelt Hospital, New York, NY; the Institute of Human Nutrition and Department of Medicine, College of Physicians and Surgeons, Columbia University; New York, NY (DG and NS); and the Obesity and Nutrition Research Center, University of Pittsburgh, Pittsburgh, PA (DEK).
2 Supported in part by NIH grants RO1-HL-70298 (diabetic data) and grants DK-PO1-42618, DK-40414, RR-00645, P30-DK-26687, and P30-DK-46204 (control data). NS was the recipient of a minority fellowship from the National Heart, Lung, and Blood Institute.
3 Reprints not available. Address correspondence to D Gallagher, Body Composition Unit–New York Obesity Research Center, St Luke's–Roosevelt Hospital, 1111 Amsterdam Avenue, Scrymser Basement, New York, NY 10025. E-mail: dg108{at}columbia.edu.
and the MRI Ancillary Study Group of the Look AHEAD Research Group
ABSTRACT
Background: The extent to which adipose tissue distribution is different between persons with type 2 diabetes (T2DM) and nondiabetic control subjects remains unclear.
Objective: The aim of this study was to establish whether total body adiposity and its distribution, quantified by using state-of-art whole-body magnetic resonance imaging, differs between these 2 groups.
Design: This cross-sectional evaluation included 93 participants (n = 56 women and 37 men) in the Look AHEAD (Action for HEAlth in Diabetes) Trial with T2DM who had a mean (±SD) age of 58.3 ± 6.6 y and body mass index (in kg/m2) of 31.6 ± 3.1 and 93 healthy nonT2DM control subjects (n = 64 women and 29 men) who had a mean (±SD) age of 60.6 ± 17.1 y and body mass index of 29.6 ± 3.0. All participants self-reported being of African American or white ancestry. Magnetic resonance imaging–derived in vivo measures of total-body AT (TAT) and its distribution, subcutaneous AT (SAT), visceral AT (VAT), and intermuscular AT (IMAT) were acquired. Linear regression models were developed for each AT compartment to adjust for important covariates of race, sex, age, height, and weight and to examine potential interactions of covariates.
Results: These models showed significantly less SAT (African American: –1.2 kg; white: –2.4 kg; both P = 0.001), including less femoral-gluteal SAT, more VAT (African American: 0.7 kg, P < 0.001; white: 1.8 kg, P = 0.007), and more IMAT (0.5 kg, P = 0.001) in the T2DM group.
Conclusion: We concluded that AT distribution is significantly altered in T2DM, ie, more VAT and IMAT—2 depots known to exacerbate insulin resistance—and less SAT in persons with T2DM than in healthy control subjects, a novel finding that we posit may compound the risk of insulin resistance.
Received for publication September 10, 2008. Accepted for publication December 17, 2008.
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