Chokeberry attenuates the expression of genes related to de novo lipogenesis in the hepatocytes of mice with nonalcoholic fatty liver disease

Nutr Res. 2016 Jan;36(1):57-64. doi: 10.1016/j.nutres.2015.10.010. Epub 2015 Oct 31.

Abstract

Nonalcoholic fatty liver disease (NAFLD), which is characterized by steatosis, is a major public health concern. Previous studies have shown that chokeberry has anti-inflammatory, antimutagenic, hepatoprotective, cardioprotective, and antidiabetic effects. In this study, we hypothesized that chokeberry powder can attenuate the expression of genes related to de novo lipogenesis and the triglyceride levels in the hepatocytes of mice with high-fat diet-induced NAFLD. After coadministering chokeberry powder for 8weeks (0.5% and 1% powder) with a high-fat diet, mice that consumed chokeberry powder diets, regardless of the dose, had significantly lower liver triglyceride levels than control mice that were fed a high-fat diet (P=.0145 and P<.0012, respectively). Compared with mice that were fed a high-fat diet, mice that were given 1% chokeberry powder exhibited significantly decreased mRNA expression of sterol regulatory element-binding protein (P=.009) and acetyl-CoA carboxylase (P=.0032) in the liver. Compared with mice in the control group, fatty acid synthase (FAS) expression significantly increased in the mice that were fed a high-fat diet, but both chokeberry powder-treated groups had significantly decreased FAS expression (P=.0157 and P<.0001, respectively). The size of the fat droplets was decreased in the livers of the chokeberry-supplemented groups. In summary, the administration of chokeberry powder may help attenuate high-fat diet-induced NAFLD by regulating the expression levels of sterol regulatory element-binding protein, acetyl-CoA carboxylase, and FAS and by decreasing the size of the fat droplets in the liver.

Keywords: Aronia melanocarpa; Chokeberry; De novo lipogenesis; High-fat diet; Lipid metabolism; Nonalcoholic fatty liver disease.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetyl-CoA Carboxylase / antagonists & inhibitors
  • Acetyl-CoA Carboxylase / genetics
  • Acetyl-CoA Carboxylase / metabolism
  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / administration & dosage
  • Anti-Inflammatory Agents, Non-Steroidal / isolation & purification
  • Anti-Inflammatory Agents, Non-Steroidal / therapeutic use*
  • Diet, High-Fat / adverse effects
  • Dietary Supplements*
  • Down-Regulation
  • Fatty Acid Synthases / antagonists & inhibitors
  • Fatty Acid Synthases / genetics
  • Fatty Acid Synthases / metabolism
  • Fruit / chemistry
  • Gene Expression Regulation*
  • Hepatocytes / immunology
  • Hepatocytes / metabolism*
  • Hepatocytes / pathology
  • Humans
  • Lipid Droplets / pathology
  • Lipogenesis*
  • Male
  • Medicine, Traditional
  • Mice, Inbred C57BL
  • Non-alcoholic Fatty Liver Disease / immunology
  • Non-alcoholic Fatty Liver Disease / metabolism
  • Non-alcoholic Fatty Liver Disease / pathology
  • Non-alcoholic Fatty Liver Disease / prevention & control*
  • Organelle Size
  • Photinia / chemistry*
  • Random Allocation
  • Sterol Regulatory Element Binding Protein 1 / antagonists & inhibitors
  • Sterol Regulatory Element Binding Protein 1 / genetics
  • Sterol Regulatory Element Binding Protein 1 / metabolism
  • Triglycerides / metabolism

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Srebf1 protein, mouse
  • Sterol Regulatory Element Binding Protein 1
  • Triglycerides
  • Fatty Acid Synthases
  • Acetyl-CoA Carboxylase