Bilberry Anthocyanins Ameliorate NAFLD by Improving Dyslipidemia and Gut Microbiome Dysbiosis.

Hironobu Nakano,Santos Garcia,De-Xing Hou,Jianhua He,Taichi Hara,Kalidas Shetty,Kozue Sakao,Shusong Wu

doi:10.3390/nu12113252

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a manifestation of metabolic syndrome closely linked to dyslipidemia and gut microbiome dysbiosis. Bilberry anthocyanins (BA) have been reported to have preventive effects against metabolic syndrome. This study aimed to investigate the protective effects and mechanisms of BA in a Western diet (WD)-induced mouse model. The results revealed that supplementation with BA attenuated the serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), low-density lipoprotein cholesterol (LDL-c), fat content in liver, 2-thiobarbituric acid reactive substances (TBARS) and α-smooth muscle actin (α-SMA) caused by WD. Furthermore, gut microbiota characterized by 16S rRNA sequencing revealed that BA reduced remarkably the ratio of Firmicutes/Bacteroidetes (F/B) and modified gut microbiome. In particular, BA increased the relative abundance of g_Akkermansia and g_Parabacteroides. Taken together, our data demonstrated that BA might ameliorate WD-induced NAFLD by attenuating dyslipidemia and gut microbiome dysbiosis.

Highlights

Non-alcoholic fatty liver disease (NAFLD) is a condition in which excess fat is stored in the liver without significant alcohol consumption
The final body weight, liver weight, epididymis fat weight, the ratio of liver weight/body weight, liver fat weight as well as total feces fat of mice fed with Western diet (WD) at 18 weeks was significantly higher than the mice fed with normal diet (ND) (Table 1)
Supplementation with Bilberry anthocyanins (BA) decreased significantly WD-enhanced all of these items except epididymis fat weight (Table 1)

Summary

Introduction

Non-alcoholic fatty liver disease (NAFLD) is a condition in which excess fat is stored in the liver without significant alcohol consumption. It embraces a pathological spectrum from simple steatosis to steatohepatitis; 10–20% have steatohepatitis (non-alcoholic steatohepatitis: NASH), which can progress to cirrhosis and hepatocellular carcinoma [1,2]. To 24.7% in USA and North America, 24% in Europe, and from 23% to 26% in Japan [3]. NAFLD is closely associated with type 2 diabetes and obesity, and both of these conditions drive progressive disease toward the more advanced stages. The mechanisms that govern hepatic lipid accumulation and the predisposition to inflammation and fibrosis are still not fully understood but reflect a complex interplay between metabolic target tissues including adipose, immune and inflammatory cells [4].

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