Granulocyte-colony stimulating factor prevents the development of hepatic steatosis in rats

Ann Hepatol. 2015 Mar-Apr;14(2):243-50.

Abstract

Background and aims: Previously, we reported that granulocyte-colony stimulating factor (G-CSF) improves hepatic steatosis in experimental animals. It may also have preventive effects on the development of hepatic steatosis. Therefore, we investigated the preventive effects of G-CSF by using a high-fat diet (HFD) rat model.

Materials and methods: Twelve rats were fed HFD and 6 rats were fed control diet from 10 weeks of age. Once little steatosis was confirmed in the liver (after 10 weeks of feeding the HFD; at 20 weeks of age), HFD rats were randomly divided into two groups and treated with either G-CSF (100 μg kg-1 day-1 for 5 consecutive days every other week; HFD/G-CSF rats) or saline (HFD/saline rats) for 10 weeks at 20 weeks of age. All rats were sacrificed at 30 weeks of age. Histology was examined by hematoxylin and eosin (H-E) and Oil Red O staining, and the expression levels of genes of associated with lipogenesis and β-oxidation enzymes were determined by qRT-PCR.

Results: Histological examinations revealed that HFD/G-CSF rats had significantly lower lipid accumulation in their hepatocytes than did HFD/saline rats (p < 0.05). HFD/G-CSF rats also showed lower expression levels of genes associated with lipogenesis and higher expression levels of genes associated with β-oxidation than HFD/saline rats (p < 0.05).

Conclusion: In conclusion, we found that G-CSF prevented development of hepatic steatosis in an HFD rat model. The preventive effect may be associated with the regulation of gene expression involved in hepatic lipogenesis and β-oxidation.

MeSH terms

  • Animals
  • Diet, High-Fat
  • Disease Models, Animal
  • Gene Expression Regulation
  • Granulocyte Colony-Stimulating Factor / pharmacology*
  • Humans
  • Lipid Metabolism / drug effects*
  • Lipid Metabolism / genetics
  • Lipogenesis / drug effects
  • Liver / drug effects*
  • Liver / metabolism
  • Liver / pathology
  • Male
  • Non-alcoholic Fatty Liver Disease / etiology
  • Non-alcoholic Fatty Liver Disease / genetics
  • Non-alcoholic Fatty Liver Disease / metabolism
  • Non-alcoholic Fatty Liver Disease / pathology
  • Non-alcoholic Fatty Liver Disease / prevention & control*
  • Oxidation-Reduction
  • Rats, Sprague-Dawley
  • Receptors, Granulocyte Colony-Stimulating Factor / agonists
  • Receptors, Granulocyte Colony-Stimulating Factor / metabolism
  • Recombinant Proteins / pharmacology
  • Time Factors

Substances

  • Receptors, Granulocyte Colony-Stimulating Factor
  • Recombinant Proteins
  • Granulocyte Colony-Stimulating Factor