Abstract

Metabolic-associated fatty liver disease (MAFLD) is the most important cause of liver disease worldwide. It is characterized by the accumulation of fat in the liver and is closely associated with abdominal obesity. In addition, oxidative stress and inflammation are significant features involved in MAFLD. Recently, our group demonstrated that lupin protein hydrolysates (LPHs) had lipid lowering, antioxidant, and anti-inflammatory effects. Sixty male mice fed with a Western diet were intragastrically treated with LPHs (or vehicle) for 12 weeks. Liver and adipose tissue lipid accumulation and hepatic inflammatory and oxidant status were evaluated. A significant decrease in steatosis was observed in LPHs-treated mice, which presented a decreased gene expression of CD36 and LDL-R, crucial markers in MAFLD. In addition, LPHs increased the hepatic total antioxidant capacity and reduced the hepatic inflammatory status. Moreover, LPHs-treated mice showed a significant reduction in abdominal adiposity. This is the first study to show that the supplementation with LPHs markedly ameliorates the generation of the steatotic liver caused by the intake of a Western diet and reduces abdominal obesity in ApoE−/− mice. Future clinical trials should shed light on the effects of LPHs on MAFLD.

Highlights

  • Metabolic-associated fatty liver disease (MAFLD) is the principal cause of chronic liver disease worldwide, with an estimated global prevalence of 25–30% [1,2]

  • WD+lupin protein hydrolysates (LPHs) mice showed a similar frequency of large adipocytes and mean area, diameter and volume per adipocyte (Figure 2F–I) to the standard diet (SD) group

  • C) To confirm the reduction of LPHs-induced steatosis, oil red staining was performed in expression was significantly reduced in LPHs-treated mice in comparison to the WD

Read more

Summary

Introduction

Metabolic-associated fatty liver disease (MAFLD) is the principal cause of chronic liver disease worldwide, with an estimated global prevalence of 25–30% [1,2]. MAFLD is associated with metabolic risk factors such as insulin resistance, hyperlipidemia and central obesity [3]. MAFLD prevalence can range 67–91% in obese subjects, depending on the BMI and waist circumference [4]. MAFLD presents a wide spectrum of clinical phenotypes that range from simple steatosis (SS) to non-alcoholic steatohepatitis (NASH) [5]. SS is characterized by the presence of more than 5% lipids in hepatocytes while NASH is characterized by advanced steatosis, ballooning, and lobular inflammation [6]. NASH may progress to fibrosis, hepatic cirrhosis, and to hepatocellular carcinoma, which can end up with the need for a liver transplant [5]

Objectives
Results
Conclusion
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call