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Provedor de dados:  Rev. Bras. Ciênc. Avic.
País:  Brazil
Título:  Molecular Characterization of Goose Phosphoenolpyruvate Carboxylase Kinase 1 (Pepck) Gene and Its Potential Role in Hepatic Steatosis Induced by Overfeeding
Autores:  Tang,B
Yang,C
Hu,S
Sun,W
Pan,Z
Li,L
Wang,J
Data:  2020-01-01
Ano:  2020
Palavras-chave:  Goose
PEPCK
Sequence characteristics
Hepatic steatosis
Primary hepatocytes
Resumo:  ABSTRACT Over-accumulation of triglycerides (TGs) in goose hepatocytes leads to the formation of fatty acid liver. Phosphoenolpyruvate carboxylase kinase 1 (PEPCK) is regarded as the rate-limiting enzyme for gluconeogenesis, and there is evidence that PEPCK is involved in regulating hepatic glucolipid metabolism. Hence, we proposed that PEPCK may have a role in goose hepatic steatosis. To test our hypothesis, the present study was conducted to firstly determine the sequence characteristics of goose PEPCK and then to explore its role in overfeeding-induced fatty liver. Our results showed that goose PEPCK encodes a 622-amino-acids protein that contains highly conserved oxaloacetate-binding domain, kinase-1 and kinase-2 motifs. PEPCK had higher mRNA levels in goose liver, and overfeeding markedly increased its expression in livers of both Sichuan White and Landes geese (p<0.05). Besides, expression of PEPCK was positively correlated with hepatic TG levels as well as plasma glucose and insulin concentrations. Additionally, in cultured goose primary hepatocyte, treatment with either oleic acid (0.8, 1.2 or 1.6 mM) or linoleic acid (0.125 or 0.25 mM) significantly (p<0.05) enhanced the expression of PEPCK. Taken together, these data suggested a role for PEPCK in the occurrence of overfeeding-induced goose hepatic steatosis.
Tipo:  Info:eu-repo/semantics/article
Idioma:  Inglês
Identificador:  http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1516-635X2020000400302
Editor:  Fundação APINCO de Ciência e Tecnologia Avícolas
Relação:  10.1590/1806-9061-2019-1128
Formato:  text/html
Fonte:  Brazilian Journal of Poultry Science v.22 n.4 2020
Direitos:  info:eu-repo/semantics/openAccess
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