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Am J Clin Nutr. 2009 Dec;90(6):1525-31. doi: 10.3945/ajcn.2009.28103. Epub 2009 Oct 14.

Dual-energy X-ray absorptiometry modeling to explain the increased resting energy expenditure associated with the HIV lipoatrophy syndrome.

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  • 1Departments of Medicine and Biostatistics and Informatics, Colorado School of Public Health, University of Colorado, Denver, Denver, CO, USA.

Abstract

BACKGROUND:

The HIV lipoatrophy syndrome is characterized by loss of subcutaneous fat and is associated with increased resting energy expenditure (REE). Recently, dual-energy X-ray absorptiometry (DXA) modeling of organ-tissue mass combined with specific organ-tissue metabolic rates has been used to gain further insight into the relation of the lean body mass to REE and to better understand differences in REE between groups.

OBJECTIVE:

This study examined the organ-tissue basis of the increased REE shown in HIV lipoatrophy.

DESIGN:

REE was measured in 29 HIV-infected patients with lipoatrophy and in 29 HIV-infected and 19 healthy control subjects. Five organ-tissue mass components (brain, bone, skeletal muscle, adipose tissue, and residual mass) were calculated with the use of DXA modeling and body weight.

RESULTS:

DXA modeling showed no significant differences in predicted REE between the 3 groups. However, measured REE was significantly greater in subjects with lipoatrophy than in control subjects. Measured REE remained significantly greater in lipoatrophy subjects after routine adjustment for lean body mass and after adjustment for each organ-tissue mass component. Finally, DXA and regression modeling of REE suggests that increased energy expenditure in skeletal muscle may account for the resting hypermetabolism of patients with HIV lipoatrophy.

CONCLUSIONS:

Increased REE in subjects with HIV lipoatrophy cannot be explained by differences in organ-tissue mass as modeled by DXA. Instead, DXA and regression modeling of REE suggests that skeletal muscle is hypermetabolic in patients with HIV lipoatrophy. This may be a form of adaptive thermogenesis in response to an inability to store triglyceride fuel in a normal manner.

PMID:
19828707
[PubMed - indexed for MEDLINE]
PMCID:
PMC2777466
Free PMC Article

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