Association of Skeletal Muscle and Adipose Tissue Distribution with Histologic Severity of Non-Alcoholic Fatty Liver.

Min-Kyu Kang,Jung-Hun Baek,Hye-Won Lee,Gyeonghwa Kim,Soo-Young Park,Won-Young Tak,Young-Oh Kweon,Jung-Gil Park,Joon-Hyuk Choi,Se-Young Jang,Keun Hur,Yu-Rim Lee,Man-Hoon Han

doi:10.3390/diagnostics11061061

Abstract

Adipose tissue and skeletal muscle is associated with non-alcoholic fatty liver disease (NAFLD). This study evaluates the association between body composition and histologic severity in patients with NAFLD. Using the cross-sectional CT images at the level of L3 vertebra and the histologic findings of 178 patients with biopsy-proven NAFLD, we analyzed the correlation of the histologic findings to the skeletal muscle index (SMI), subcutaneous adipose tissue index (SATI), and visceral adipose tissue index (VATI), which is defined as the body composition area (cm2) by height squared (m2). The clinical and laboratory features with body composition were analyzed to determine the risk factors for advanced fibrosis. The VATI significantly increased in severe non-alcoholic steatohepatitis (NASH) or advanced fibrosis. In addition, the VATI was correlated with the NAFLD activity score (NAS) and the fibrosis stage. In multivariate analyses, age (odds ratio (OR), 1.09; 95% confidence interval (CI), 1.02–1.19; p = 0.025), severe NASH (OR, 8.66; 95% CI, 2.13–46.40; p = 0.005), and visceral adiposity (OR, 6.77; 95% CI, 1.81–29.90; p = 0.007) were independently associated with advanced fibrosis in patients with NAFLD. Visceral adiposity is correlated with the histologic severity of NAFLD, which is independently associated with advanced fibrosis.

Highlights

The incidence of non-alcoholic fatty liver disease (NAFLD), one of the most important chronic liver diseases, has been increasing in obese people over the past three decades [1]
The spectrum of NAFLD ranges from simple steatosis to non-alcoholic steatohepatitis (NASH), which leads to cirrhosis and hepatocellular carcinoma [3]
We believe that skeletal muscle loss was associated with lobular inflammation of the liver and commitment obesity acts synergistically, subsequently affecting NAFLD progression

Summary

Introduction

The incidence of non-alcoholic fatty liver disease (NAFLD), one of the most important chronic liver diseases, has been increasing in obese people over the past three decades [1]. As a variable clinical manifestation, fat accumulation in the visceral organs harboring genetic polymorphism was considered as a subtype of NAFLD without obesity [6]. Regardless of obesity, visceral adipose tissue (VAT) is associated with MetS and T2D [7]. A positive energy balance induces fat accumulation in the subcutaneous adipose tissue (SAT), which has a relatively lesser effect on insulin resistance (IR) at the initial stage of NAFLD [9]. When adipose tissue dysfunction with intolerance of energy excess develops, fat is accumulated in the visceral organs, including the liver, heart, skeletal muscle, and VAT [10]. Crosstalk between the liver, adipose tissue, and pro-inflammatory molecules, such as interleukin-6 (IL-6) and tumor necrosis factor-α, released from activated macrophages and adipokines plays a pivotal role in NAFLD progression [12]

Methods

Results

Conclusion