Growth hormone enhances fat-free mass and glutamine availability in patients with short-bowel syndrome: an ancillary
David Seguy1, Dominique Darmaun1, Alain Duhamel1
1From the Service de Nutrition Lille, France (DS); the Institut National de la Santé et de la Recherche Médicale, Lille, Unité U995, Université Lille Nord de France, Lille, France (DS and FG); the Département de Biostatistiques, Equipe d'Accueil EA2694, Lille, France (AD); the Centre Hospitalier Régional Universitaire de Lille, Université Lille Nord de France, Lille, France (DS, AD, AC, and FG); the Institut National de la Recherche Agronomique Unité Mixte de Recherche 1280, Centre de Recherche en Nutrition Humaine, Université de Nantes, Nantes, France (DD); the Laboratoire de Biochimie, Centre Hospitalier, Meaux, France (FT); the Service Interhospitalier de Biochimie Cochin, Assistance Publique-Hôpitaux de Paris et Equipe d'Accueil EA4466, Faculté de Pharmacie, Université Paris Descartes, Paris, France (LC); and the Université Paris 7 Denis Diderot, Paris, France (BM).
Background:
Benefits of recombinant human growth hormone (rhGH) alone or combined with glutamine in patients with intestinal failure because of short-bowel syndrome remain controversial.
Objective:
We explored effects of rhGH on whole-body protein metabolism in patients with short-bowel syndrome with intestinal failure (SBS-IF) to gain insight into its mechanism of action.
Design:
Eight stable hyperphagic patients with severe SBS-IF received, in a double-blind, randomized crossover study, low-dose rhGH (0.05 mg · kg⁻¹ · d⁻¹) and a placebo for two 3-wk periods. Leucine and glutamine kinetics under fasting and fed conditions, fat-free mass (FFM), and serum insulin were determined on the final day of each treatment.
Results:
rhGH increased FFM and nonoxidative leucine disposal (NOLD; an index of protein synthesis) (P < 0.02), whereas FFM and NOLD were correlated in the fed state (r = 0.81, P = 0.015). With rhGH administration, leucine release from protein breakdown (an index of proteolysis) decreased in the fed compared with fasting states (P = 0.012), which was not observed with the placebo. However, the fast-to-fed difference in leucine release from protein breakdown was not significantly different between rhGH and placebo (P = 0.093). With rhGH, the intestinal absorption of leucine and glutamine increased (P = 0.036) and correlated with serum insulin (r = 0.91, P = 0.002). rhGH increased glutamine de novo synthesis (P < 0.02) and plasma concentrations (P < 0.03) in both fasting and fed states.
Conclusions:
In SBS-IF patients, feeding fails to decrease proteolysis in contrast to what is physiologically observed in healthy subjects. rhGH enhances FFM through the stimulation of protein synthesis and might decrease proteolysis in response to feeding. Improvements in de novo synthesis and intestinal absorption increase glutamine availability over the physiologic range, suggesting that beneficial effects of rhGH in hyperphagic patients might be achieved without glutamine supplementation.
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