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Effect of propionate, pyruvate and β-hydroxybutyric acid on pyruvate carboxylase mRNA expression of in vitro culture bovine hepatocytes

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ABSTRACT

The objective was to detect the effect of propionate, pyruvate and β-hydroxybutyric acid on pyruvate carboxylase mRNA expression in in vitro culture bovine hepatocytes through a quantity reverse transcription polymerase chain reaction method. Pyruvate carboxylase is a key enzyme in the liver gluconeogenesis of ruminants and plays an important role in the negative energy balance of peri-parturient dairy cows. The effect of propionate, pyruvate and β-hydroxybutyric acid on pyruvate carboxylase mRNA expression at cell level is presented in this article. In experiment 1, the various concentrations of propionate from 0 mmol/L to 11.5 mmol/L, were added to the hepatocytes media. The results indicate that the level of pyruvate carboxylase mRNA was significantly enhanced accompanying increased propionate concentrations in the media (P < 0.01) and high concentrations of propionate did not inhibit the levels of pyruvate carboxylase mRNA. In experiment 2, pyruvate in concentrations from 0 mmol/L to 12 mmol/L was added to the media. The results indicate that the levels of pyruvate carboxylase mRNA were significantly enhanced when concentrations of pyruvate increased from 0 mmol/M to 4 mmol/M and decreased when concentrations of pyruvate increased from 8 mmol/M to 12 mmol/M (P < 0.01). In experiment 3, β-hydroxybutyric acid of various concentrations from 0 mmol/L to 3.0 mmol/L was added to the media. The results indicate that pyruvate carboxylase mRNA levels increased slightly when concentrations of β-hydroxybutyric acid were less than 1 mmol/L, and pyruvate carboxylase mRNA levels decreased significantly when they exceeded 2 mmol/L or 3 mmol/L (P < 0.01). There results suggest that β-hydroxybutyric acid inhibits PC mRNA expression.
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Keywords: hepatocytes; propionate; pyruvate; pyruvate carboxylase mRNA; β-hydroxybutyric acid

Document Type: Research Article

Publication date: August 1, 2006

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