Abstract
We measured aminotransferase activity and vitamin B6 content in the livers of diabetic mice. Two different types of diabetic mice, spontaneously non-obese diabetic (NOD) and alloxan-induced diabetic (Allo) mice, were used. Control mice were either non-diabetic NOD or ICR. We have reported a marked increase in aspartate aminotransferase (AST) activity in the liver of diabetic mice compared with that in control mice. The diabetic livers also had more vitamin B6 than normal livers ; pyridoxamine (PM) levels were particularly high but pyridoxal levels were not. The abundance of AST and B6 in the diabetic liver is consistent with the great need for gluconeogenic substrate there. This is understandable in that most aminotransferases require vitamin B6. A correlation between s-AST and PM was recognized in the diabetic liver, while AST and PM were negatively correlated in normal mice. A metabolic shift towards gluconeogenesis apparently produces more B6 and PM while it induces holo-AST synthesis.