Granulocyte-colony stimulating factor prevents the development of hepatic steatosis in rats
- Authors
- Song, Yi-Sun; Joo, Hyun-Woo; Park, In-Hwa; Shen, Guang-Yin; Lee, Yonggu; Shin, Jeong Hun; Kim, Hyuck; Kim, Kyung-Soo
- Issue Date
- Mar-2015
- Publisher
- MEXICAN ASSOC HEPATOLOGY
- Keywords
- High-fat diet; Lipogenesis; beta-oxidation
- Citation
- ANNALS OF HEPATOLOGY, v.14, no.2, pp.243 - 250
- Indexed
- SCIE
SCOPUS
- Journal Title
- ANNALS OF HEPATOLOGY
- Volume
- 14
- Number
- 2
- Start Page
- 243
- End Page
- 250
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/157822
- DOI
- 10.1016/S1665-2681(19)30787-2
- ISSN
- 1665-2681
- 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 mu g 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 0 staining, and the expression levels of genes of associated with lipogenesis and beta-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 beta-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 beta-oxidation.
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