Abstract

Many studies have shown that resistant maltodextrin (RMD) possesses blood cholesterol lowering and anti-obesity effects. In order to investigate the effect of RMD on lipid metabolism in the liver, rats were fed with a high-fat (HF) diet for 7 weeks to induce hyperlipidemia and fatty liver. Normal control rats were fed with a normal diet. HF-diet-fed rats were treated with 5% RMD for 8 weeks. The results showed that the increased plasma aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities, the increased hepatic triglyceride and total cholesterol levels, and fatty liver in HF-diet-fed rats were significantly decreased after supplementation with RMD. Supplementation with RMD significantly (1) induced AMP-activated protein kinase (AMPK) phosphorylation; (2) inhibited the activities of acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), and HMG-CoA reductase (HMGCR); (3) suppressed the protein expression of peroxisome proliferator activated receptor (PPAR)-γ; (4) increased β-oxidation of fatty acids by increasing the protein expression carnitine palmitoyl transferase 1α (CPT-1α) in the livers of HF-diet-fed rats. Taken together, supplementation of RMD was capable of inhibiting lipogenic enzyme activities and inducing fatty acid β-oxidation through increasing AMPK activation, thereby reducing lipid accumulation in the liver.

Highlights

  • Lack of physical activity and excessive calorie intake creates an energy imbalance in the human body

  • Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease, which is characterized by hepatic lipid accumulation

  • These results indicate that resistant maltodextrin (RMD) is capable of improving the alterations of lipogenic enzymes and lipid metabolism-related signaling molecules in the livers of HF-diet-fed rats

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Summary

Introduction

Lack of physical activity and excessive calorie intake creates an energy imbalance in the human body. Sugars and lipids in the diet are metabolized in the body to triglyceride (TG) and accumulate in the adipose tissue and liver, which may cause obesity and fatty liver. Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease, which is characterized by hepatic lipid accumulation. The prevalence of NAFLD in the adult population in Taiwan is as high as 33.6% [1]. The causes of NAFLD include drugs, obesity, diabetes, and hyperlipidemia to induce non-alcohol liver injury, which may eventually evolve into non-alcoholic steatohepatitis (NASH), liver fibrosis, liver cirrhosis, and liver failure or liver cancer [2].

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