title: Anabolic effects of recombinant human growth hormone in patients with wasting associated with human immunodeficiency virus infection.
abstract: Body wasting, characterized by disproportionate loss of body cell mass, is a feature of many chronic diseases, including infection with the human immunodeficiency virus (HIV). Therapies that merely increase energy intake do not consistently restore body cell mass in patients with the wasting syndrome. Because treatment with GH has induced nitrogen (N) retention in catabolic patients after surgery, burns, cancer, and hypocaloric feeding, we designed this study to determine whether GH could also produce an anabolic response in persons with HIV-associated weight loss. Six HIV-positive (HIV+) men with an average weight loss of 19% and six healthy weight-stable controls (HIV-) were hospitalized on a metabolic ward, where they consumed a constant metabolic diet during successive 5-day precontrol, 7-day baseline, and 7-day treatment [recombinant human GH (rhGH), 0.1 mg/kg.day] periods. The effects of rhGH on body weight, N and electrolyte excretion, energy expenditure, substrate oxidation, and integrated lipid and carbohydrate metabolism were assessed. Body weight increased promptly and progressively during treatment (2.0 +/- 0.3 and 1.6 +/- 0.2 kg in HIV+ and HIV-, respectively). Urinary N excretion decreased by 288 +/- 17 and 287 +/- 42 mmol/day in HIV+ and HIV-, respectively. Resting energy expenditure increased by 7.5% in both groups. Protein oxidation decreased, whereas lipid oxidation increased significantly. Glucose flux increased, and modest increases in fasting plasma triglyceride, glucose, and insulin levels were observed. Thus, short term rhGH treatment increased both protein anabolism and protein-sparing lipid oxidation, effects that should increase body cell mass if sustained during chronic therapy.
authors.affiliation: Division of Endocrinology, San Francisco General Hospital, California 94110.
authors.forename: K
authors.initials: K
authors.lastname: Mulligan
authors.forename: C
authors.initials: C
authors.lastname: Grunfeld
authors.forename: M K
authors.initials: MK
authors.lastname: Hellerstein
authors.forename: R A
authors.initials: RA
authors.lastname: Neese
authors.forename: M
authors.initials: M
authors.lastname: Schambelan
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D001786:Blood Glucose / Q000032:analysis; D004614:Emaciation / Q000188:drug therapy / Q000209:etiology*; D004734:Energy Metabolism / Q000187:drug effects; D013006:Growth Hormone / Q000494:pharmacology* / Q000627:therapeutic use; D015658:HIV Infections / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D006801:Humans; D007328:Insulin / Q000097:blood; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D008055:Lipids / Q000097:blood; D008297:Male; D009584:Nitrogen / Q000652:urine; D010084:Oxidation-Reduction; D011188:Potassium / Q000097:blood / Q000652:urine; D011994:Recombinant Proteins / Q000494:pharmacology / Q000627:therapeutic use; D012964:Sodium / Q000097:blood / Q000652:urine; D014508:Urea / Q000652:urine; D015431:Weight Loss / Q000187:drug effects*
chemical_list: D001786:Blood Glucose; D007328:Insulin; D008055:Lipids; D011994:Recombinant Proteins; D007334:Insulin-Like Growth Factor I; D014508:Urea; D013006:Growth Hormone; D012964:Sodium; D009584:Nitrogen; D011188:Potassium