Delving into disability in Crohn's disease: Dysregulation of molecular pathways may explain skeletal muscle loss in Crohn's disease☆

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Abstract

Background/aims

In Crohn's disease (CD), skeletal muscle mass and function are reduced compared to healthy controls, potentially resulting in disability. Mechanisms contributing to muscle impairment, and thus potential therapeutic targets, are poorly understood. This study aimed to measure and compare skeletal muscle size and molecular targets involved in skeletal muscle growth, in CD subjects and healthy controls.

Methods

CD (n = 27) and healthy (n = 22) subjects were recruited from the IBD outpatient clinic and via local advertisement respectively. Demographics and clinical data were collected via survey and interview. Quadriceps muscle cross-sectional area was measured using peripheral quantitative CT scanning. Levels of muscle hypertrophy and atrophy signalling targets using quantitative PCR and western blotting were measured in muscle biopsies.

Results

Muscle size was 14% lower (p = 0.055) and a 54% lower phosphorylated:total (p:t) Akt ratio was measured in the muscle samples (p < 0.05), indicating an attenuated muscle hypertrophy pathway in CD compared with controls. In those with CD, a lower p:t Akt ratio (< 0.97) was associated with lower serum vitamin D3, lower physical activity indices (49 vs 64 mmol/L, 1.7 vs 2.2 × 106 accelerometer counts respectively, each p < 0.05) and a trend towards lower serum ferritin levels (128 vs 322 mg/L, p = 0.07), compared with CD subjects with normal/high p:t Akt ratios.

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