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Association between telomere length and hepatic fibrosis in non-alcoholic fatty liver disease.

ABSTRACT: Telomere length has been linked to the prevalence and progression of metabolic disease. However, clinical implications of telomere length in biopsy-proven non-alcoholic fatty liver disease (NAFLD) patients remain unclear. Therefore, this study aimed to investigate the association of telomere length with the histological severity of NAFLD. The cross-sectional data derived from the prospectively enrolled Boramae NAFLD registry (n = 91) were analyzed. The liver tissues and clinical information were obtained from both NAFLD patients and non-NAFLD subjects. Binary logistic regression was performed to identify the independent association between telomere length and the histological severity of NAFLD. A total of 83 subjects with or without biopsy-proven NAFLD were included for analysis: non-NAFLD in 23 (27.7%), non-alcoholic fatty liver in 15 (18.1%), and non-alcoholic steatohepatitis (NASH) in 45 (54.2%). Telomere length measured from liver tissues showed a strong negative correlation (p < 0.001) with age, regardless of NAFLD status. Therefore, telomere length was corrected for age. Age-adjusted telomere length than decreased gradually with an increasing severity of fibrosis in patients with NAFLD (p < 0.028). In multivariate analysis, age-adjusted telomere length (odds ratio [OR] 0.59; 95% CI 0.37-0.92; p = 0.019) and high-density lipoprotein cholesterol (OR 0.94; 95% CI 0.80-0.99; p = 0.039) were independently associated with significant fibrosis. The age-adjusted telomere length tends to decrease along with the fibrosis stage of NAFLD. In particular, among the histological components of NAFLD, fibrosis severity seems to be related to telomere length in the liver.

SUBMITTER: Shin HK

PROVIDER: S-EPMC8429461 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description: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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Association between telomere length and hepatic fibrosis in non-alcoholic fatty liver disease.

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