Nachit Maxime, Lanthier Nicolas, Rodriguez Julie, Neyrinck Audrey M, Cani Patrice D, Bindels Laure B, Hiel Sophie, Pachikian Barbara D, Trefois Pierre, Thissen Jean-Paul, Delzenne Nathalie M
Laboratory of Hepato-Gastroenterology, Institut de Recherche Expérimentale et Clinique, UCLouvain, Université catholique de Louvain, Brussels, Belgium.
Department of Imaging and Pathology, KU Leuven, Leuven, Belgium.
JHEP Rep. 2021 Jun 15;3(4):100323. doi: 10.1016/j.jhepr.2021.100323. eCollection 2021 Aug.
BACKGROUND & AIMS: Retrospective cross-sectional studies linked sarcopenia and myosteatosis with metabolic dysfunction-associated fatty liver disease (MAFLD). Here, we wanted to clarify the dynamic relationship between sarcopenia, myosteatosis, and MAFLD.
A cohort of 48 obese patients was randomised for a dietary intervention consisting of 16 g/day of inulin (prebiotic) or maltodextrin (placebo) supplementation. Before and after the intervention, we evaluated liver steatosis and stiffness with transient elastography (TE); we assessed skeletal muscle index (SMI) and skeletal muscle fat index (SMFI) (a surrogate for absolute fat content in muscle) using computed tomography (CT) and bioelectrical impedance analysis (BIA).
At baseline, sarcopenia was uncommon in patients with MAFLD (4/48, 8.3%). SMFI was higher in patients with high liver stiffness than in those with low liver stiffness (640.6 ± 114.3 cm/ Hounsfield unit [HU] . 507.9 ± 103.0 cm/HU, = 0.001). In multivariate analysis, SMFI was robustly associated with liver stiffness even when adjusted for multiple confounders (binary logistic regression, <0.05). After intervention, patients with inulin supplementation lost weight, but this was not associated with a decrease in liver stiffness. Remarkably, upon intervention (being inulin or maltodextrin), patients who lowered their SMFI, but not those who increased SMI, had a 12.7% decrease in liver stiffness (before = 6.36 ± 2.15 . after = 5.55 ± 1.97 kPa, = 0.04).
Myosteatosis, but not sarcopenia, is strongly and independently associated with liver stiffness in obese patients with MAFLD. After intervention, patients in which the degree of myosteatosis decreased reduced their liver stiffness, irrespective of body weight loss or prebiotic treatment. The potential contribution of myosteatosis to liver disease progression should be investigated.
NCT03852069.
The fat content in skeletal muscles (or myosteatosis) is strongly associated with liver stiffness in obese patients with MAFLD. After a dietary intervention, patients in which the degree of myosteatosis decreased also reduced their liver stiffness. The potential contribution of myosteatosis to liver disease progression should be investigated.
回顾性横断面研究将肌肉减少症和肌脂肪变性与代谢功能障碍相关脂肪性肝病(MAFLD)联系起来。在此,我们旨在阐明肌肉减少症、肌脂肪变性与MAFLD之间的动态关系。
将48名肥胖患者随机分为两组,分别进行饮食干预,一组每天补充16克菊粉(益生元),另一组补充麦芽糊精(安慰剂)。在干预前后,我们使用瞬时弹性成像(TE)评估肝脏脂肪变性和硬度;使用计算机断层扫描(CT)和生物电阻抗分析(BIA)评估骨骼肌指数(SMI)和骨骼肌脂肪指数(SMFI,肌肉中绝对脂肪含量的替代指标)。
在基线时,MAFLD患者中肌肉减少症并不常见(4/48,8.3%)。肝脏硬度高的患者的SMFI高于肝脏硬度低的患者(640.6±114.3厘米/亨氏单位[HU]对507.9±103.0厘米/HU,P=0.001)。在多变量分析中,即使在调整了多个混杂因素后,SMFI仍与肝脏硬度密切相关(二元逻辑回归,P<0.05)。干预后,补充菊粉的患者体重减轻,但这与肝脏硬度降低无关。值得注意的是,在干预后(无论是菊粉还是麦芽糊精),SMFI降低的患者肝脏硬度下降了12.7%,而SMI增加的患者则没有(干预前=6.36±2.15,干预后=5.55±1.97千帕,P=0.04)。
在患有MAFLD的肥胖患者中,肌脂肪变性而非肌肉减少症与肝脏硬度密切且独立相关。干预后,肌脂肪变性程度降低的患者肝脏硬度降低,无论体重减轻与否或是否接受益生元治疗。应研究肌脂肪变性对肝病进展的潜在影响。
NCT03852069。
骨骼肌中的脂肪含量(即肌脂肪变性)与患有MAFLD的肥胖患者的肝脏硬度密切相关。饮食干预后,肌脂肪变性程度降低的患者肝脏硬度也降低。应研究肌脂肪变性对肝病进展的潜在影响。