title: Physiologic growth hormone replacement improves fasting lipid kinetics in patients with HIV lipodystrophy syndrome.
abstract: 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.
  
  
  METHODS
  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 microg x kg(-1) x d(-1)).
  
  
  RESULTS
  GH replacement decreased the rates of total lipolysis [FFA(total) rate of appearance (x +/- SE): from 4.80 +/- 1.24 to 3.32 +/- 0.76 mmol FFA x kg fat(-1) x h(-1); P < 0.05] and net lipolysis (FFA(net) rate of appearance: from 1.87 +/- 0.34 to 1.20 +/- 0.25 mmol FFA x kg fat(-1) x h(-1); P < 0.05). Fat oxidation decreased (from 0.28 +/- 0.02 to 0.20 +/- 0.02 mmol FFA x kg lean body mass(-1) x 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 x kg fat(-1) x 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.
authors.affiliation: Translational Metabolism Unit and the Division of Diabetes, Endocrinology and Metabolism, Department of Medicine, Baylor College of Medicine, Houston, TX 77030-2600, USA.
authors.forename: Susana
authors.initials: S
authors.lastname: D'Amico
authors.forename: Jianjian
authors.initials: J
authors.lastname: Shi
authors.forename: Rajagopal V
authors.initials: RV
authors.lastname: Sekhar
authors.forename: Farook
authors.initials: F
authors.lastname: Jahoor
authors.forename: Kenneth J
authors.initials: KJ
authors.lastname: Ellis
authors.forename: Khaleel
authors.initials: K
authors.lastname: Rehman
authors.forename: James
authors.initials: J
authors.lastname: Willis
authors.forename: Mario
authors.initials: M
authors.lastname: Maldonado
authors.forename: Ashok
authors.initials: A
authors.lastname: Balasubramanyam
mesh_terms: D017667:Adipocytes / Q000378:metabolism; D053299:Apolipoprotein B-100; D001055:Apolipoproteins B / Q000096:biosynthesis / Q000097:blood; D001823:Body Composition; D002247:Carbon Isotopes; D003903:Deuterium; D004951:Esterification; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D039682:HIV-Associated Lipodystrophy Syndrome / Q000378:metabolism*; D019382:Human Growth Hormone / Q000172:deficiency* / Q000494:pharmacology*; D006801:Humans; D050356:Lipid Metabolism / Q000187:drug effects*; D008066:Lipolysis / Q000187:drug effects*; D008099:Liver / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010084:Oxidation-Reduction; D010168:Palmitates / Q000378:metabolism
chemical_list: D053299:Apolipoprotein B-100; D001055:Apolipoproteins B; D002247:Carbon Isotopes; D005230:Fatty Acids, Nonesterified; D010168:Palmitates; D019382:Human Growth Hormone; D003903:Deuterium