Muscle Function is Associated With Presence, New-onset, or Worsening of Hepatic Steatosis Assessed by Biochemical Parameters, Independent of Muscle Mass

Non-alcoholic fatty liver disease (NAFLD) becomes a major health problem leading to metabolic complications and end-stage liver disease, lacking effective therapeutic interventions. Skeletal muscle deficit, or sarcopenia, is related to accelerated accumulation of ectopic fat at liver. Skeletal muscle can be a novel intervention target of NAFLD. However, previous studies focused on the association between muscle mass and NAFLD, whereas the association of muscle function with NAFLD, a more clinically relevant assessment regarding skeletal muscle, remains unclear. Among participants enrolled between 2013 to 2014 in cardiovascular and Metabolic Diseases Etiology Research Center (CMERC) study (n=807), a cohort of community-dwelling Korean adults to study cardiovascular risk factors, a total of 500 individuals were recruited for 5-year follow-up. Hepatic steatosis was defined by hepatic steatosis index 36 or higher (HSI=8X(AST/ALT)+BMI+2 [if diabetes]+2 [if female]). New-onset of hepatic steatosis was defined as newly developed hepatic steatosis at current follow-up compared to baseline and worsening of HSI was defined as the highest quartile of HSI changes (2 or higher HSI increase). Muscle function was assessed by peak countermovement jump power relative weight (W/kg), 5 times chair rise test (CRT; in seconds), and grip strength (GS; in kg). Appendicular lean mass (ALM) was measured using bioimpedance analysis (InBody770, Biospace, Seoul, Korea). A total of 439 subjects (women 74%; mean age 57 ± 8 year) were analyzed after excluding those with excessive alcohol intake (n=51) and any missing values (n=10). Hepatic steatosis was present in 40% of subjects, which was increased from baseline period (33%, p<0.001). Low peak jump power (adjusted odds ratio [aOR] 1.14 per 1 W/kg decrease), GS (aOR 1.08 per 1kg decrease), and CRT performance (aOR 1.09 per 1 second increase; p<0.05 for all) were all associated with elevated odds of hepatic steatosis, after adjustment for age, gender, height, ALM, and metabolic syndrome components. Compared to those without hepatic steatosis at baseline and follow-up, those with persistent hepatic steatosis had significantly lower jump power in both men and women (33 vs. 40 W/kg in men, p=0.027; 26 vs. 29 W/kg in women, p<0.001). Jump power remained as robust predictor for new-onset hepatic steatosis or worsening of HSI (aOR 1.05 per 1W/kg decrease, p=0.044), whereas GS, CRT, and ALM were not. Muscle function measured by jump power was associated with presence or worsening of hepatic steatosis assessed by biochemical parameters, independent of muscle mass. Acknowledgement: We thank CMERC participants and all research staffs for this work. Funding: This study was supported by research grants from Hanmi Pharmaceutical Co.,Ltd. (4-2018-0845).