Amanda Davies1, Aline Nixon1, Rafeeq Muhammed2, Kostas Tsintzas1, Sian Kirkham3, Francis B Stephens4, Gordon W Moran5. 1. Faculty of Medicine and Health Sciences, University of Nottingham, Nottingham, United Kingdom. 2. Birmingham Women's and Children's NHS Foundation Trust, Birmingham, United Kingdom. 3. Nottingham Children's Hospital, Nottingham University Hospitals, Nottingham, United Kingdom. 4. Sport and Health Sciences, University of Exeter, Exeter, United Kingdom. 5. Nottingham Digestive Diseases Centre, University of Nottingham, Nottingham, United Kingdom; National Institute of Health Research Nottingham Biomedical Research Centre at the Nottingham University Hospitals and University of Nottingham, Nottingham, United Kingdom. Electronic address: Gordon.Moran@nottingham.ac.uk.
Abstract
BACKGROUND & AIMS: An inability to respond to nutrition could be implicated in low muscle mass in Crohn's disease. We aim to determine skeletal muscle metabolic response to feeding in Crohn's disease and healthy volunteers. METHODS: Twenty asymptomatic Crohn's disease participants (15.6 ± 0.5 yrs; BMI 20.6 ± 0.9 kg/m2); 9 with active disease (faecal calprotectin, 808 ± 225 ug/g and C-reactive protein, 2.2 ± 1.2 mg/dl), 11 in deep remission (faecal calprotectin, 61 ± 12 ug/g and C-reactive protein, 0.3 ± 0.2 mg/dl) and 9 matched healthy volunteers (16.0 ± 0.6 yrs; BMI 20.7 ± 0.6 kg/m2) were recruited. Participants had a dual energy X-ray absorptiometry scan, handgrip dynamometer test, wore a pedometer and completed a food diary. Arterialised hand and venous forearm blood samples were collected concurrently and brachial artery blood flow measured at baseline and every 20 min for 2 hrs after the ingestion of a standardised liquid meal. Net balance of branched chain amino acids (BCAA) and glucose were derived. RESULTS: Controls had a positive mean BCAA balance. CD participants had an initial anabolic response to the meal, with increasing BCAA balance between t = 0 & t = 20, but returned to negative by t = 60. This was associated with reduced FFM z-scores in CD but not with insulin resistance or disease activity. Exploratory analyses suggest that negative postprandial BCAA response seen in CD is predominant in males (p = 0.049), with associated lower appendicular muscle mass (p = 0.034), higher muscle fatigue (p = 0.014) and reduced protein intake (p = 0.026). CONCLUSIONS: The inability to sustain a positive protein balance postprandially could provide an explanation for the reduced muscle mass seen in CD. Further mechanistic studies will be needed to confirm these findings.
BACKGROUND & AIMS: An inability to respond to nutrition could be implicated in low muscle mass in Crohn's disease. We aim to determine skeletal muscle metabolic response to feeding in Crohn's disease and healthy volunteers. METHODS: Twenty asymptomatic Crohn's diseaseparticipants (15.6 ± 0.5 yrs; BMI 20.6 ± 0.9 kg/m2); 9 with active disease (faecal calprotectin, 808 ± 225 ug/g and C-reactive protein, 2.2 ± 1.2 mg/dl), 11 in deep remission (faecal calprotectin, 61 ± 12 ug/g and C-reactive protein, 0.3 ± 0.2 mg/dl) and 9 matched healthy volunteers (16.0 ± 0.6 yrs; BMI 20.7 ± 0.6 kg/m2) were recruited. Participants had a dual energy X-ray absorptiometry scan, handgrip dynamometer test, wore a pedometer and completed a food diary. Arterialised hand and venous forearm blood samples were collected concurrently and brachial artery blood flow measured at baseline and every 20 min for 2 hrs after the ingestion of a standardised liquid meal. Net balance of branched chain amino acids (BCAA) and glucose were derived. RESULTS: Controls had a positive mean BCAA balance. CDparticipants had an initial anabolic response to the meal, with increasing BCAA balance between t = 0 & t = 20, but returned to negative by t = 60. This was associated with reduced FFM z-scores in CD but not with insulin resistance or disease activity. Exploratory analyses suggest that negative postprandial BCAA response seen in CD is predominant in males (p = 0.049), with associated lower appendicular muscle mass (p = 0.034), higher muscle fatigue (p = 0.014) and reduced protein intake (p = 0.026). CONCLUSIONS: The inability to sustain a positive protein balance postprandially could provide an explanation for the reduced muscle mass seen in CD. Further mechanistic studies will be needed to confirm these findings.
Authors: Antoinette A Amevor; Toshifumi Yodoshi; Andrew T Trout; Jonathan R Dillman; Ruchi Singh; Ryan Jarvis; Lin Fei; Chunyan Liu; Amy Taylor; Alexander Miethke; Marialena Mouzaki Journal: Liver Int Date: 2021-11-29 Impact factor: 8.754