Abstract

BackgroundWe investigated the association between muscle strength and the prevalence of advanced fibrosis among individuals with non‐alcoholic fatty liver disease (NAFLD) using a nationwide cross‐sectional survey.MethodsIndividuals, 20 to 79 years of age, from the Korean National Health and Nutrition Examination Surveys (KNHANES) from 2014 to 2016 were selected (N = 14 861), with sample weights applied. Muscle strength was quantified as the handgrip strength divided by the body mass index (BMI); low muscle strength (LMS) was defined as the lowest quartile (Q1) of the handgrip strength/BMI for our sample population. NAFLD was defined as hepatic steatosis index >36. Advanced fibrosis was defined as a fibrosis‐4 index score ≥1.30 (FibrosisFIB4).ResultsThe mean age of the study population was 45.6 ± 0.2 years, and 42.4% were male. As muscle strength increased, the mean BMI and age decreased accordingly, and the proportions of diabetes, dyslipidaemia, hypertension, and obesity decreased significantly (P < 0.001 for all). In a crude analysis, the LMS was associated with an increased prevalence of NAFLD (odds ratio [OR] 3.62, 95% confidence interval [CI] 3.25–4.03, P < 0.001), which remained significant even after adjustment for age, sex, obesity, insulin resistance, diabetes, hypertension, dyslipidaemia, and high‐sensitivity C‐reactive protein (OR 1.66, 95% CI 1.28–2.16, P < 0.001). In this logistic regression model, the prevalence of NAFLD decreased by 24% with each quartile increment in muscle strength (OR 0.76, 95% CI 0.68–0.85, P < 0.001). Among individuals with NAFLD (n = 2092), LMS was significantly associated with the presence of advanced fibrosis (FibrosisFIB4) independently of age, sex, obesity, diabetes, hypertension, dyslipidaemia, and high‐sensitivity C‐reactive protein (OR 1.66, 95% CI 1.01–2.49, P = 0.015), which lost its statistical significance after additional adjustment for insulin resistance.ConclusionsLow muscle strength is independently associated with NAFLD. The significant association between LMS and advanced fibrosis in NAFLD may be mediated through insulin resistance.

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