title: Growth hormone blunts protein oxidation and promotes protein turnover to a similar extent in abdominally obese and normal-weight women.
abstract: Abdominally obese individuals have reduced 24-h plasma GH concentrations. Their normal plasma IGF-I levels may reflect GH hypersensitivity. Alternatively, obesity-associated hyposomatotropism may cause less biological effect in target tissues. We therefore determined whole-body responsiveness to the anabolic effects of GH in abdominally obese (OB) and normal weight (NW) premenopausal women. A 1-h iv infusion of GH or placebo was randomly administered to six NW (body mass index, 21.1 +/- 1.9 kg/m(2)) and six OB (body mass index, 35.5 +/- 1.5 kg/m(2)) women in a cross-over design. Endogenous insulin, glucagon and GH secretion was suppressed by infusion of somatostatin. Whole-body protein turnover was measured using a 10-h infusion of [(13)C]-leucine. GH administration induced a similar plasma GH peak in NW and OB women (49.8 +/- 10.4 vs. 45.1 +/- 5.6 mU/liter). GH, compared with placebo infusion, increased nonoxidative leucine disposal, P < 0.0001) and endogenous leucine appearance (R(a), P = 0.0004) but decreased leucine oxidation (P = 0.0051). All changes were similar in both groups. Accordingly, whole-body GH responsiveness, defined as the maximum response of nonoxidative leucine disposal, leucine R(a), and oxidation per unit of GH, was not different in OB and NW women (0.25 +/- 0.18 vs. 0.19 +/- 0.17 micro mol/kg.h, 0.21 +/- 0.23 vs. 0.13 +/- 0.17 micro mol/kg.h, and -0.10 +/- 0.08 vs. -0.08 +/- 0.05 micro mol/kg.h, respectively). These results indicated that whole-body tissue responsiveness to the net anabolic effect of GH is similar in OB and NW women. Hence, we inferred that hyposomatotropism may promote amino acid oxidation and blunt protein turnover in abdominal obesity. However, hyposomatotropism cannot account for all anomalous features of protein metabolism in abdominally obese humans.
authors.affiliation: Department of General Internal Medicine, Leiden University Medical Centre, 2300 RC Leiden, The Netherlands. m.m.buijs@lumc.edu
authors.forename: Madelon M
authors.initials: MM
authors.lastname: Buijs
authors.forename: Johannes A
authors.initials: JA
authors.lastname: Romijn
authors.forename: Jacobus
authors.initials: J
authors.lastname: Burggraaf
authors.forename: Marieke L
authors.initials: ML
authors.lastname: De Kam
authors.forename: Adam F
authors.initials: AF
authors.lastname: Cohen
authors.forename: Marijke
authors.initials: M
authors.lastname: Frölich
authors.forename: Frans
authors.initials: F
authors.lastname: Stellaard
authors.forename: A Edo
authors.initials: AE
authors.lastname: Meinders
authors.forename: Hanno
authors.initials: H
authors.lastname: Pijl
mesh_terms: D000005:Abdomen; D000328:Adult; D018592:Cross-Over Studies; D004311:Double-Blind Method; D005260:Female; D013006:Growth Hormone / Q000494:pharmacology*; D006728:Hormones / Q000097:blood; D006801:Humans; D007930:Leucine / Q000378:metabolism*; D009765:Obesity / Q000378:metabolism*; D009994:Osmolar Concentration; D010084:Oxidation-Reduction / Q000187:drug effects; D012016:Reference Values; D013004:Somatostatin / Q000494:pharmacology
chemical_list: D006728:Hormones; D013004:Somatostatin; D013006:Growth Hormone; D007930:Leucine