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Am J Physiol Endocrinol Metab 283: E332-E337, 2002. First published April 23, 2002; doi:10.1152/ajpendo.00058.2002
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Vol. 283, Issue 2, E332-E337, August 2002

Metabolic basis of HIV-lipodystrophy syndrome

Rajagopal V. Sekhar1,4, Farook Jahoor4, A. Clinton White2,5, Henry J. Pownall3, Fehmida Visnegarwala2, Maria C. Rodriguez-Barradas2, Morali Sharma1,5, Peter J. Reeds4, and Ashok Balasubramanyam1,5

Sections of 1 Endocrinology, 2 Infectious Diseases, and 3 Atherosclerosis, Department of Medicine, and 4 Department of Pediatrics, Children's Nutrition Research Center and US Department of Agriculture/Agricultural Research Service, Baylor College of Medicine, Houston 77030; and 5 Ben Taub General Hospital, Houston, Texas 77030

Human immunodeficiency virus (HIV)-lipodystrophy syndrome (HLS) is characterized by hypertriglyceridemia, low high-density lipoprotein-cholesterol, lipoatrophy, and central adiposity. We investigated fasting lipid metabolism in six men with HLS and six non-HIV-infected controls. Compared with controls, HLS patients had lower fat mass (15.9 ± 1.3 vs. 22.3 ± 1.7 kg, P < 0.05) but higher plasma glycerol rate of appearance (Ra), an index of total lipolysis (964.71 ± 103.33 vs. 611.08 ± 63.38 µmol · kg fat-1 · h-1, P < 0.05), Ra palmitate, an index of net lipolysis (731.49 ± 72.36 vs. 419.72 ± 33.78 µmol · kg fat-1 · h-1, P < 0.01), Ra free fatty acids (2,094.74 ± 182.18 vs. 1,470.87 ± 202.80 µmol · kg fat-1 · h-1, P < 0.05), and rates of intra-adipocyte (799.40 ± 157.69 vs. 362.36 ± 74.87 µmol · kg fat-1 · h-1, P < 0.01) and intrahepatic fatty acid reesterification (1,352.08 ± 123.90 vs. 955.56 ± 124.09 µmol · kg fat-1 · h-1, P < 0.05). Resting energy expenditure was increased in HLS patients (30.51 ± 2.53 vs. 25.34 ± 1.04 kcal · kg lean body mass-1 · day-1, P < 0.05), associated with increased non-plasma-derived fatty acid oxidation (139.04 ± 24.17 vs. 47.87 ± 18.81 µmol · kg lean body mass-1 · min-1, P < 0.02). The lipoatrophy observed in HIV lipodystrophy is associated with accelerated lipolysis. Increased hepatic reesterification promotes the hypertriglyceridemia observed in this syndrome.

lipolysis; hypertriglyceridemia; very low density lipoprotein; high-density lipoprotein-cholesterol


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