Literature DB >> 25650070

Formoterol, a highly β2-selective agonist, induces gender-dimorphic whole body leucine metabolism in humans.

Paul Lee1, Vita Birzniece2, A Margot Umpleby3, Anne Poljak4, Ken K Y Ho5.   

Abstract

OBJECTIVE: Formoterol is a β(2)-selective agonist that enhances protein anabolism in rodents. Whether formoterol imparts anabolic benefits in humans is unknown. The objective of the study was to investigate the effects of formoterol on whole body protein rates of turnover, oxidative loss and synthesis.
DESIGN: Open label intervention study. PATIENTS: Fifteen healthy adults (8 men). MEASUREMENTS: Volunteers were treated with oral formoterol 160 μg/day for one week. Changes in leucine turnover (LRa; index of protein breakdown), oxidation (Lox; irreversible protein loss) and incorporation into protein (LIP; index of protein synthesis) were assessed using the whole body 1-[(13)C]leucine turnover technique before/after treatment.
RESULTS: LRa, Lox and LIP correlated significantly with lean body mass (LBM). LRa, adjusted for LBM was significantly higher (P<0.05, 160±6 vs 109±3 μmol/min) in men but not fractional Lox and LIP (expressed as a proportion of LRa). Formoterol reduced LRa (-9±4%) in men but stimulated LRa (9±3%) in women. Formoterol significantly reduced (P<0.05) fractional Lox, an effect greater in women (-4±1 vs -1±1 %). It stimulated fractional LIP in women (∆4±1%, P<0.05) but not in men (∆1±1%). Formoterol induced an absolute anabolic effect that was greater in women (30 vs 8%). Heart rate, systolic and diastolic blood pressures were unaffected.
CONCLUSION: In a therapeutic dose, formoterol stimulates protein anabolism in humans. It induced gender-dimorphic effects on protein turnover and on the partitioning of amino acids from oxidative loss toward protein synthesis, effects that are greater in women than in men. Formoterol holds promise as a treatment for sarcopenia.
Copyright © 2015 Elsevier Inc. All rights reserved.

Entities:  

Keywords:  Beta-agonist; Formoterol; Leucine turnover; Sarcopenia; Skeletal muscle

Mesh:

Substances:

Year:  2014        PMID: 25650070     DOI: 10.1016/j.metabol.2014.12.005

Source DB:  PubMed          Journal:  Metabolism        ISSN: 0026-0495            Impact factor:   8.694


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