Mechanism of Liver Tyrosine Aminotransferase Increase in Ethanol-Treated Mice and Its Effect on Serum Tyrosine Level

Abstract

Summary Liver tyrosine aminotransferase (TAT) activity is known to increase with ethanol treatment; however, the mechanism of this increase is unclear. Upon investigation we found that TAT activity and mRNA levels started to increase 2 h after ethanol administration and continued to increase until 6 h after ethanol administration. The increase in ethanol-induced TAT activity could not be explained by calorie loading after fasting, since ethanol loading increased TAT expression, while glucose loading decreased TAT expression. In addition, liver TAT activity was not related to serum tyrosine levels. TAT activity increased when an adenosine A2 agonist, 5 ¢ -N -ethylcarboxamide adenosine, was given. Since TAT activity is increased by cAMP, and ethanol increases cAMP production via an adenosine receptor-dependent mechanism, this increase in ethanol-induced TAT activity may occur via an adenosine receptor-dependent mechanism.

The Adenosine Receptor Agonist 5’-N-Ethylcarboxamide-Adenosine Increases Mouse Serum Total Homocysteine Levels, Which Is a Risk Factor for Cardiovascular Diseases

“…Total RNA was extracted using the acid guanidine thiocyanate-phenol-chloroform method [20]. Details of the northern hybridization method have been described previously [23].…”

“…We previously reported that the non-specific adenosine receptor agonist 5'-N-ethylcarboxamide-adenosine (NECA) increased serum glucose levels and the expression of a glucogenic enzyme (glucose 6-phosphatase) in the liver [19] [20]. Based on the dose of NECA administered in these studies and plasma concentrations after the administration of other adenosine agonists [21], it was inferred that the serum NECA concentration was in the μM range and also that NECA activated adenosine A2b receptors.…”

The Adenosine Receptor Agonist 5’-<i>N</i>-Ethylcarboxamide-Adenosine Increases Glucose 6-Phosphatase Expression and Gluconeogenesis

“…In our previous study, we found that in fasting mice treated with NECA for 6 h, serum glucose levels increased and serum alanine levels decreased [11]. Glucose is produced by the glucose-alanine cycle, and because serum alanine levels are decreased by NECA, it is thought that NECA stimulates gluconeogenesis.…”