Intramuscular fat in steatotic liver disease is linked to muscle function impairment, insulin resistance and specific inflammatory pathways in the liver
(2026) EASL congress — Location: Barcelona (27.May.2026)
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- (en) Background and aims: A muscle-liver axis, described on the basis of muscle density, appears to operate in cases of metabolic steatohepatitis. Here, we want to investigate the muscle phenotype (surface and intramuscular fat) by magnetic resonance imaging (MRI) in relation to muscle function and liver disease. Method: Patients with SLD with an increased liver stiffness on transient elastography (≥7.8 kPa) were prospectively recruited. They underwent liver/skeletal muscles MRI and liver biopsy on the same day. Controls underwent the same MRI protocol. Mean liver and muscles (abdominal and paravertebral muscles) fat were measured by proton density fat fraction (PDFF). Muscle mass was assessed at the third lumbar vertebrae using the skeletal muscle index (SMI). Intramyocellular (IMCL) and extramyocellular lipids (EMCL) of right soleus and tibialis anterior were quantified using proton magnetic resonance spectroscopy. Muscle strength was assessed by the Liver Frailty Index (LFI). Liver biopsies were used for both histology and bulk mRNA sequencing. Results: Patients with SLD (n = 92, 54 MASLD, 38 ALD) and controls (n = 10) were comparable for age. Ballooning was identified in 50% and fibrosis was graded as ≥ 2 in 63% of the SLD cohort. Median liver PDFF (19% vs. 3%, p < 0.001), mean muscle PDFF (22% vs. 9%, p < 0.001) and mean SMI (54 cm2 /m2 vs. 36 cm2 /m2, p < 0.001) were higher in the SLD group compared to controls. Despite significant metabolic differences such as BMI or presence of type 2 diabetes, muscle PDFF, LFI and SMI were similar in MASLD and ALD groups. Participants with SLD and high muscle PDFF (>30%) showed decreased muscle strength compared to participants with low PDFF (<30%) but comparable age and BMI in both sexes. No correlation was found however between EMCL, IMCL and the liver frailty index while insulin resistance specifically correlated to soleus EMCL in MASLD (r = 0.72, p = 0.005) but not in ALD. Finally, transcriptomic analysis reveals that muscle fat is associated with an upregulation of hepatic inflammatory pathways and a downregulation of bile acid synthesis and fatty acid degradation. Conclusion: Muscle fat assessed by MRI is increased in the presence of SLD and is associated with decreased muscle strength. EMCL are linked to insulin resistance in MASLD. Mechanistically, this disruption of the muscle-liver axis is associated with hepatic transcriptional changes including upregulated inflammatory pathways and downregulated bile acid biosynthesis and fatty acid degradation.
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Henin, G., Nachit, M., André-Dumont, S., Goffaux, A., Declerck, S., Gouw, A., Sempoux, C., Baldin, P., Henry, P., Duchene, G., Trefois, P., Danse, E., Reyngoudt, H., Marty, B., Ambroise, J., Loumaye, A., Starkel, P., Leclercq, I., Lanthier, N., & et al. (2026). Intramuscular fat in steatotic liver disease is linked to muscle function impairment, insulin resistance and specific inflammatory pathways in the liver. Journal of Hepatology. Supplement, 84(S1), S648-649. https://doi.org/10.1016/S0168-8278(26)01807-6 (Original work published 2026)