Butyrate supplementation reduces sarcopenia by repairing neuromuscular junction in patients with chronic obstructive pulmonary disease.

Butyrate Chronic obstructive pulmonary disease Neuromuscular junction Sarcopenia

Journal

Respiratory medicine
ISSN: 1532-3064
Titre abrégé: Respir Med
Pays: England
ID NLM: 8908438

Informations de publication

Date de publication:
20 Dec 2023
Historique:
received: 16 11 2023
revised: 14 12 2023
accepted: 20 12 2023
medline: 23 12 2023
pubmed: 23 12 2023
entrez: 22 12 2023
Statut: aheadofprint

Résumé

Chronic obstructive pulmonary disease (COPD) is associated with an intestinal leak and neuromuscular junction (NMJ) degradation, which contributes to physical compromise and accelerated age-related muscle loss, called sarcopenia. However, the relevant interventions partly remain ineffective. We investigated the effects of exogenous butyrate on sarcopenia and physical capacity with relevance to intestinal permeability and NMJ integrity in COPD patients. COPD patients were randomized into placebo (n = 67) and butyrate (n = 64) groups in a double-blind manner. The patients in the butyrate group received one 300mg capsule a day for 12 weeks. We measured circulating markers of intestinal leak (zonulin), systemic bacterial load (LBP), and NMJ loss (CAF22), along with handgrip strength (HGS), and short physical performance battery (SPPB) at baseline and 12 weeks. Butyrate supplementation improved HGS and gait speed in COPD patients. Among SPPB indices, butyrate improved the ability to maintain postural balance and walking and prevented a decline in the ability to rise from a chair. Butyrate also reduced the plasma levels of zonulin, LBP, and CAF22 levels in COPD patients (all p < 0.05). Regression analysis revealed significant associations of plasma zonulin and CAF22 with HGS, gait speed, and cumulative SPPB scores in butyrate group. These changes were associated with reduced markers of inflammation and muscle damage. Butyrate may provide a therapeutic approach to sarcopenia and physical dependency in COPD by repairing intestinal leak and NMJ loss.

Identifiants

pubmed: 38135194
pii: S0954-6111(23)00398-0
doi: 10.1016/j.rmed.2023.107510
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

107510

Informations de copyright

Copyright © 2023. Published by Elsevier Ltd.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that there is no conflict of interest.

Auteurs

Rizwan Qaisar (R)

Basic Medical Sciences, College of Medicine, University of Sharjah, Sharjah, 27272, United Arab Emirates; Space Medicine Research Group, Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah, 27272, United Arab Emirates; Cardiovascular Research Group, Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah, 27272, United Arab Emirates. Electronic address: rqaisar@sharjah.ac.ae.

Asima Karim (A)

Basic Medical Sciences, College of Medicine, University of Sharjah, Sharjah, 27272, United Arab Emirates.

Tahir Muhammad (T)

Department of Biochemistry, Gomal Medical College, Gomal University, Dera Ismail Khan, 30130, Pakistan.

Firdos Ahmad (F)

Basic Medical Sciences, College of Medicine, University of Sharjah, Sharjah, 27272, United Arab Emirates; Space Medicine Research Group, Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah, 27272, United Arab Emirates; Cardiovascular Research Group, Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah, 27272, United Arab Emirates.

Classifications MeSH