Abstract
Background and Objectives: Recent studies have shown that low skeletal muscle mass can contribute to non-alcoholic fatty liver disease through insulin resistance. However, the association between muscle mass/strength and hepatic fat content remains unclear in postmenopausal women. Methods: In this study, we assessed the associations between muscle mass/strength and various severities of non-alcoholic fatty liver disease. Using single-voxel proton magnetic resonance spectroscopy, 96 postmenopausal women between the ages of 50 and 65 were divided into four groups (G0–G3) by hepatic fat content: G0 (hepatic fat content <5%, n = 20), G1 (5% ≤ hepatic fat content < 10%, n = 27), G2 (10% ≤ hepatic fat content < 25%, n = 31), and G3 (hepatic fat content ≥25%, n = 18). Muscle mass indexes were estimated as skeletal muscle index (SMI)% (total lean mass/weight × 100) and appendicular skeletal muscular mass index (ASM)% (appendicular lean mass/weight × 100) by dual energy X-ray absorptiometry. Maximal isometric voluntary contraction of the handgrip, elbow flexors, and knee extensors was measured using an adjustable dynamometer chair. Fasting plasma glucose, insulin, and follicle-stimulating hormones were assessed in venous blood samples. Results: The results showed negative correlations between hepatic fat content and SMI% (r = −0.42, p < 0.001), ASM% (r = −0.29, p = 0.005), maximal voluntary force of grip (r = −0.22, p = 0.037), and knee extensors (r = −0.22, p = 0.032). Conclusions: These significant correlations almost remained unchanged even after controlling for insulin resistance. In conclusion, negative correlations exist between muscle mass/strength and the progressed severity of non-alcoholic fatty liver disease among post-menopausal women, and the correlations are independent of insulin resistance.
Highlights
The prevalence of non-alcoholic fatty liver disease (NAFLD) in China increased from 18.22%(2000–2006) to 20.86% (2010–2013) [1]
Skeletal muscle is the main site of insulin consumption, and muscular function impairment greatly contributes to the development of insulin resistance (IR) [2], which causes fatty liver disease [3]
We hypothesized that among NAFLD patients with IR, imbalanced muscle protein synthesis and proteolysis could result in the loss of muscle mass, resulting in a vicious cycle
Summary
The prevalence of non-alcoholic fatty liver disease (NAFLD) in China increased from 18.22%(2000–2006) to 20.86% (2010–2013) [1]. The prevalence of non-alcoholic fatty liver disease (NAFLD) in China increased from 18.22%. The role of skeletal muscle in NAFLD has attracted increasing attention. Skeletal muscle is the main site of insulin consumption, and muscular function impairment greatly contributes to the development of insulin resistance (IR) [2], which causes fatty liver disease [3]. As a hallmark of NAFLD, IR may downregulate the effects of insulin on maintaining muscle mass. Insulin inhibits muscle protein degradation [6] and, together with amino acids, stimulates muscle protein synthesis [7,8]. Recent studies have shown that low skeletal muscle mass can contribute to non-alcoholic fatty liver disease through insulin resistance. The association between muscle mass/strength and hepatic fat content remains unclear in postmenopausal women
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