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Am J Physiol Endocrinol Metab (April 30, 2002). doi:10.1152/ajpendo.00058.2002
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Articles in PresS, published online ahead of print April 30, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00058.2002
Submitted on February 11, 2002
Accepted on April 18, 2002

Metabolic basis of HIV-lipodystrophy syndrome

Rajagopal V Sekhar1, Farook Jahoor2, A. Clinton White3, Henry J Pownall4, Fehmida Visnegarwala4, Maria C Rodriguez-Barradas4, Morali Sharma3, Peter J Reeds2, and Ashok Balasubramanyam3*

1 Medicine, Baylor College of Medicine, Houston, TX, USA; Pediatrics, Baylor College of Medicine, Houston, TX, USA
2 Pediatrics, Baylor College of Medicine, Houston, TX, USA
3 Medicine, Baylor College of Medicine, Houston, TX, USA; Medicine, Ben Taub General Hospital, Houston, TX, USA
4 Medicine, Baylor College of Medicine, Houston, TX, USA

* To whom correspondence should be addressed. E-mail: ashokb{at}bcm.tmc.edu.

HIV-lipodystrophy syndrome (HLS) is characterized by hypertriglyceridemia, low HDL-cholesterol, lipoatrophy and central adiposity. We investigated fasting lipid metabolism in 6 men with HLS and 6 non-HIV-infected controls. Compared to controls, HLS patients had lower fat mass (15.9 ± 1.3 vs. 22.3 ± 1.7 kg [mean ± SE], P<0.05), but higher plasma Ra glycerol, an index of total lipolysis (964.71 ± 103.33 vs. 611.08 ± 63.38 µmol/kg-fat/h, P<0.05), Ra palmitate, an index of net lipolysis (731.49 ± 72.36 vs. 419.72 ± 33.78 µmol/kg-fat/h, P<0.01), Ra free fatty acids (2094.74 ± 182.18 vs. 1470.87 ± 202.80 µmol/kg-fat/h, P<0.05), and rates of intraadipocyte (799.40 ± 157.69 vs. 362.36 ± 74.87 µmol/kg-fat/h, P<0.01) and intrahepatic fatty acid reesterification (1352.08 ± 123.90 vs. 955.56 ± 124.09 mmol fatty acid/kg-fat/h, P<0.05). Resting energy expenditure was increased in HLS patients (30.51 ± 2.53 vs~. 25.34 ± 1.04 kcal/kg-LBM/d, P<0.05), associated with increased non-plasma-derived fatty acid oxidation (139.04 ± 24.17 vs. 47.87 ± 18.81 µmol/kg-LBM/min, P<0.02). The lipoatrophy observed in HIV-lipodystrophy is associated with accelerated lipolysis. Increased hepatic reesterification promotes the hypertriglyceridemia observed in this syndrome.




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