Physiologic growth hormone replacement improves fasting lipid kinetics in patients with HIV lipodystrophy syndrome

Susana D'Amico, Jianjian Shi, Rajagopal V. Sekhar, Farook Jahoor, Kenneth J. Ellis, Khaleel Rehman, James Willis, Mario Maldonado, Ashok Balasubramanyam

Research output: Contribution to journalArticle

17 Citations (Scopus)

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. Design: Seven men with HLS and GHD were studied with the use of infusions of [13C 1]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 (x- ± SE): from 4.80 ± 1.24 to 3.32 ± 0.76 mmol FFA·kg fat-1·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·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.

Original languageEnglish (US)
Pages (from-to)204-211
Number of pages8
JournalAmerican Journal of Clinical Nutrition
Volume84
Issue number1
StatePublished - Jul 1 2006
Externally publishedYes

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HIV-Associated Lipodystrophy Syndrome
somatotropin
Growth Hormone
fasting
Fasting
Lipolysis
Lipids
kinetics
lipolysis
Fats
lipids
Apolipoprotein B-100
apolipoprotein B-100
Palmitates
palmitates
Nonesterified Fatty Acids
oxidation
free fatty acids
Waist-Hip Ratio
Liver

Keywords

  • Adipocyte
  • Dyslipidemia
  • Fat redistribution
  • Insulin resistance

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Food Science

Cite this

D'Amico, S., Shi, J., Sekhar, R. V., Jahoor, F., Ellis, K. J., Rehman, K., ... Balasubramanyam, A. (2006). Physiologic growth hormone replacement improves fasting lipid kinetics in patients with HIV lipodystrophy syndrome. American Journal of Clinical Nutrition, 84(1), 204-211.

Physiologic growth hormone replacement improves fasting lipid kinetics in patients with HIV lipodystrophy syndrome. / D'Amico, Susana; Shi, Jianjian; Sekhar, Rajagopal V.; Jahoor, Farook; Ellis, Kenneth J.; Rehman, Khaleel; Willis, James; Maldonado, Mario; Balasubramanyam, Ashok.

In: American Journal of Clinical Nutrition, Vol. 84, No. 1, 01.07.2006, p. 204-211.

Research output: Contribution to journalArticle

D'Amico, S, Shi, J, Sekhar, RV, Jahoor, F, Ellis, KJ, Rehman, K, Willis, J, Maldonado, M & Balasubramanyam, A 2006, 'Physiologic growth hormone replacement improves fasting lipid kinetics in patients with HIV lipodystrophy syndrome', American Journal of Clinical Nutrition, vol. 84, no. 1, pp. 204-211.
D'Amico, Susana ; Shi, Jianjian ; Sekhar, Rajagopal V. ; Jahoor, Farook ; Ellis, Kenneth J. ; Rehman, Khaleel ; Willis, James ; Maldonado, Mario ; Balasubramanyam, Ashok. / Physiologic growth hormone replacement improves fasting lipid kinetics in patients with HIV lipodystrophy syndrome. In: American Journal of Clinical Nutrition. 2006 ; Vol. 84, No. 1. pp. 204-211.
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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. Design: Seven men with HLS and GHD were studied with the use of infusions of [13C 1]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 (x- ± SE): from 4.80 ± 1.24 to 3.32 ± 0.76 mmol FFA·kg fat-1·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·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.",
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author = "Susana D'Amico and Jianjian Shi and Sekhar, {Rajagopal V.} and Farook Jahoor and Ellis, {Kenneth J.} and Khaleel Rehman and James Willis and Mario Maldonado and Ashok Balasubramanyam",
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AU - Shi, Jianjian

AU - Sekhar, Rajagopal V.

AU - Jahoor, Farook

AU - Ellis, Kenneth J.

AU - Rehman, Khaleel

AU - Willis, James

AU - Maldonado, Mario

AU - Balasubramanyam, Ashok

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N2 - 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 [13C 1]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 (x- ± SE): from 4.80 ± 1.24 to 3.32 ± 0.76 mmol FFA·kg fat-1·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·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.

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