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ORIGINAL RESEARCH COMMUNICATION |
1 From the Translational Metabolism Unit and the Division of Diabetes, Endocrinology and Metabolism, Department of Medicine (SD, JS, RVS, KR, MM, and AB); the Department of Pediatrics and the US Department of Agriculture/Agricultural Research Service Children's Nutrition Research Center (FJ and KJE); and the Department of Radiology (JW), Baylor College of Medicine, Houston, TX; and the Endocrine Service, Ben Taub General Hospital, Houston, TX (RVS, MM, and AB)
Background: HIV lipodystrophy syndrome (HLS) is characterized by accelerated lipolysis, inadequate fat oxidation, increased hepatic reesterification, and a high frequency of growth hormone deficiency (GHD). The effect of growth hormone (GH) replacement on these lipid kinetic abnormalities is unknown.
Objective: We aimed to measure the effects of physiologic GH replacement on lipid kinetics in men with HLS and GHD.
Design: Seven men with HLS and GHD were studied with the use of infusions of [13C1]palmitate, [2H5]glycerol, and [2H3]leucine to quantify total and net lipolysis, palmitate and free fatty acid (FFA) oxidation, and VLDL apolipoprotein B-100 synthesis before and after 6 mo of GH replacement (maximum: 5 µg · kg–1 · d–1).
Results: GH replacement decreased the rates of total lipolysis [FFAtotal rate of appearance (
± SE): from 4.80 ± 1.24 to 3.32 ± 0.76 mmol FFA · kg fat–1 · h–1; P < 0.05] and net lipolysis (FFAnet rate of appearance: from 1.87 ± 0.34 to 1.20 ± 0.25 mmol FFA · kg fat–1 · h–1; P < 0.05). Fat oxidation decreased (from 0.28 ± 0.02 to 0.20 ± 0.02 mmol FFA · kg lean body mass–1 · h–1; P < 0.002), as did the rate of appearance of FFAs available for intrahepatic reesterification (from 0.50 ± 0.13 to 0.29 ± 0.09 mmol FFA · kg fat–1 · h–1; P < 0.03). Fractional and absolute synthetic rates of VLDL apolipoprotein B-100 were unaltered. These kinetic changes were associated with a decrease in the waist-to-hip ratio but no significant change in fasting plasma lipid concentrations. Fasting plasma glucose concentrations increased after treatment (from 5.2 ± 0.2 to 5.8 ± 0.3 mmol/L; P < 0.01).
Conclusions: Physiologic GH replacement has salutary effects on abnormal lipid kinetics in HLS. The effects are mediated by diminished lipolysis and hepatic reesterification rather than by increased fat oxidation.
Key Words: Dyslipidemia • insulin resistance • fat redistribution • adipocyte
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