Abstract
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.
Highlights
Gluconeogenesis is a process through which non-carbohydrate sources, such as lactic acid, allyl alcohol, amino acids, and glycerol, can be converted into glucose or glycogen (Chakravarty et al, 2007)
Following the conversion of non-carbohydrate sources to oxaloacetate (OAA) during the process of tricarboxylic acid cycle (TCA), PEPCK catalyzes the conversion of OAA into phosphoenolpyruvate (PEP) (Montal et al, 2015), indicating that PEPCK may play a role in regulating hepatic glucose and lipid metabolism
Subcellular localization prediction suggested that goose PEPCK protein was mainly located in the Molecular Characterization of Goose Phosphoenolpyruvate Carboxylase Kinase 1 (Pepck) Gene and Its Potential Role in Hepatic Steatosis Induced by Overfeeding cytoplasm
Summary
Gluconeogenesis is a process through which non-carbohydrate sources, such as lactic acid, allyl alcohol, amino acids, and glycerol, can be converted into glucose or glycogen (Chakravarty et al, 2007). Following the conversion of non-carbohydrate sources to oxaloacetate (OAA) during the process of tricarboxylic acid cycle (TCA), PEPCK catalyzes the conversion of OAA into phosphoenolpyruvate (PEP) (Montal et al, 2015), indicating that PEPCK may play a role in regulating hepatic glucose and lipid metabolism. Increasing evidence has shown that PEPCK is crucial for hepatic glyceroneogenesis. A previous study reported that downregulation of PEPCK mRNA in diabetic (db/db) mice by RNAi led to decrease plasma glucose, insulin, and TG concentrations (Gómez-Valadés et al, 2008). Liver-specific knockout of mice PEPCK significantly promoted gluconeogenesis and increased hepatic glycogen output, but resulted eRBCA-2019-1128
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