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Ann Hepatol ; 14(2): 243-50, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-25671834

RESUMO

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 ß-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 ß-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 ß-oxidation.


Assuntos
Fator Estimulador de Colônias de Granulócitos/farmacologia , Metabolismo dos Lipídeos/efeitos dos fármacos , Fígado/efeitos dos fármacos , Hepatopatia Gordurosa não Alcoólica/prevenção & controle , Animais , Dieta Hiperlipídica , Modelos Animais de Doenças , Regulação da Expressão Gênica , Humanos , Metabolismo dos Lipídeos/genética , Lipogênese/efeitos dos fármacos , Fígado/metabolismo , Fígado/patologia , Masculino , Hepatopatia Gordurosa não Alcoólica/etiologia , Hepatopatia Gordurosa não Alcoólica/genética , Hepatopatia Gordurosa não Alcoólica/metabolismo , Hepatopatia Gordurosa não Alcoólica/patologia , Oxirredução , Ratos Sprague-Dawley , Receptores de Fator Estimulador de Colônias de Granulócitos/agonistas , Receptores de Fator Estimulador de Colônias de Granulócitos/metabolismo , Proteínas Recombinantes/farmacologia , Fatores de Tempo
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