Hepatoprotective Effects of Insect Extracts in an Animal Model of Nonalcoholic Fatty Liver Disease.

A-Rang Im,Sungwook Chae,Seung Hyung Kim,Won-Kyung Yang,Yang-Chun Park

doi:10.3390/nu10060735

Abstract

Insects represent the largest and most diverse group of organisms on earth and are potential food and drug resources. Recently, we have demonstrated that a Forsythia viridissima extract prevented free fatty acid-induced lipid accumulation in an in vitro cellular nonalcoholic fatty liver disease (NAFLD) model. In this study, we aimed to evaluate the hepatoprotective effects of extracts of the insects Protaetia brevitarsis seulensis Kolbe, 1886 (PB), Oxya chinensis sinuosa Mishchenko, 1951 (OC), and Gryllus bimaculatus De Geer, 1773 (GB) in a high-fat diet (HFD)-induced NAFLD animal model, as well as to elucidate the underlying mechanisms. The effects of the supplementation with PB, OC, and GB extracts were evaluated histopathologically and histochemically. PB, OC, and GB extract supplementation inhibited the HFD-induced increase in body weight and body fat mass and ameliorated other adverse changes, resulting in decreased liver function parameters, lower serum triglyceride and cholesterol levels, and increased serum adiponectin levels. The expression of hepatic genes involved in lipid droplet accumulation and in fatty acid uptake also decreased upon treatment of HFD-fed mice with the extracts. These results provide evidence of the protective effects of the PB, OC, and GB extracts against HFD-induced fatty liver disease in an animal model.

Highlights

Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease, which encompasses the entire spectrum of fatty liver diseases occurring in individuals in the absence of significant alcohol consumption and ranging from fatty liver to steatohepatitis and cirrhosis
The aim of our study was to evaluate the hepatoprotective effects of ethanol extracts of three insects, including P. brevitarsis seulensis (PB), O. chinensis sinuosa (OC), and G. bimaculatus (GB), in a high-fat diet (HFD)-induced animal nonalcoholic fatty liver disease (NAFLD) model, as well as to elucidate the underlying mechanisms
We evaluated whether the PB, OC, and free fatty acids (FFA)-induced lipid accumulation in mimic the excessive FFA influx into hepatocytes during NAFLD

Summary

Introduction

Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease, which encompasses the entire spectrum of fatty liver diseases occurring in individuals in the absence of significant alcohol consumption and ranging from fatty liver to steatohepatitis and cirrhosis. NAFLD is generally considered a comorbidity of obesity and a hepatic manifestation of metabolic syndrome [1,2]. NAFLD is generally considered to result from an increased delivery and uptake of free fatty acids (FFA) into hepatocytes, owing to their excessive dietary intake or release from the adipose tissue, increased de novo hepatic FFA and triglyceride (TG) synthesis, failure of very low-density lipoprotein (LDL) synthesis and TG export, or failure of FFA elimination due to impaired hepatic mitochondrial. TG synthesis is stimulated to dispose of excess FFAs, leading to excessive accumulation of hepatic TGs, which is associated with an increased supply of FFAs from the peripheral adipose tissue to the liver and to an enhanced de novo lipid synthesis via the lipogenic pathway [5]. The circulating pool of FFAs increases in obese individuals and accounts for most of liver TGs in NAFLD [6]

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