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Metabolic basis of HIV-lipodystrophy syndrome
Rajagopal V Sekhar1, Farook Jahoor, A Clinton White
1Section of Endocrinology and Department of Medicine, Children's Nutrition Research Center and US Department of Agriculture/Agricultural Research Service, Baylor College of Medicine, Houston 77030, USA.
Insights
Human immunodeficiency virus (HIV)-lipodystrophy syndrome (HLS) accelerates lipolysis, leading to fat loss and altered lipid metabolism. This study reveals increased hepatic fatty acid reesterification contributes to hypertriglyceridemia in HLS patients.
Area of Science:
- Metabolic Disorders
- Lipid Metabolism
- HIV/AIDS Complications
Background:
- Human immunodeficiency virus (HIV)-lipodystrophy syndrome (HLS) presents with dyslipidemia and body fat redistribution.
- Key features include hypertriglyceridemia, low HDL-cholesterol, lipoatrophy, and central adiposity.
Purpose of the Study:
- To investigate fasting lipid metabolism in men with HLS.
- To compare lipolysis and fatty acid metabolism between HLS patients and healthy controls.
Main Methods:
- Utilized stable isotope tracers to measure glycerol and fatty acid kinetics.
- Assessed rates of lipolysis, fatty acid reesterification, and oxidation in vivo.
- Measured resting energy expenditure and body composition.
Main Results:
- HLS patients exhibited significantly lower fat mass compared to controls.
- Increased rates of total lipolysis (glycerol R(a)) and net lipolysis (palmitate R(a)) were observed in HLS patients.
- Elevated intra-adipocyte and intrahepatic fatty acid reesterification rates were found in HLS.
- HLS patients showed increased resting energy expenditure and non-plasma-derived fatty acid oxidation.
Conclusions:
- Lipoatrophy in HIV lipodystrophy is linked to accelerated lipolysis.
- Increased hepatic fatty acid reesterification is a key mechanism driving hypertriglyceridemia in HLS.
- Metabolic alterations in HLS involve complex changes in lipid turnover and energy expenditure.
Abstract:
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 (R(a)), an index of total lipolysis (964.71 +/- 103.33 vs. 611.08 +/- 63.38 micromol x kg fat(-1) x h(-1), P < 0.05), R(a) palmitate, an index of net lipolysis (731.49 +/- 72.36 vs. 419.72 +/- 33.78 micromol x kg fat(-1) x h(-1), P < 0.01), R(a) free fatty acids (2,094.74 +/- 182.18 vs. 1,470.87 +/- 202.80 micromol x kg fat(-1) x h(-1), P < 0.05), and rates of intra-adipocyte (799.40 +/- 157.69 vs. 362.36 +/- 74.87 micromol x kg fat(-1) x h(-1), P < 0.01) and intrahepatic fatty acid reesterification (1,352.08 +/- 123.90 vs. 955.56 +/- 124.09 micromol x kg fat(-1) x h(-1), P < 0.05). Resting energy expenditure was increased in HLS patients (30.51 +/- 2.53 vs. 25.34 +/- 1.04 kcal x kg lean body mass(-1) x day(-1), P < 0.05), associated with increased non-plasma-derived fatty acid oxidation (139.04 +/- 24.17 vs. 47.87 +/- 18.81 micromol x kg lean body mass(-1) x 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.