[Guanidinoacetic acid in serum, urine and renal cortex from streptozotocin-induced diabetic rats].

Guanidinoacetic acid (GAA) is generally considered to be synthesized by glycine-amidinotransferase (GAT) in the renal tubular epithelial cells. The purpose of the present study was to determine serum, urinary and renal cortex GAA levels in streptozotocin (STZ) -induced diabetic rats with or without insulin treatment, for evaluating whether the GAA assay is a clinical marker for renal tubular dysfunction in diabetes. Urinary and serum samples, and renal cortex of the rats were obtained one, two and three weeks after the injection of 65 mg/kg of STZ. GAA and 1.5 anhydroglucitol (1. 5AG) levels were measured by HPLC. N-acetyl glucosaminidase (NAG) activity was determined by the enzymatic method. GAA levels in serum, urine and renal cortex from STZ-diabetic rats were significantly decreased compared with those of the control rats. The serum, urinary and renal cortex GAA levels were markedly ameliorated by insulin treatment. In contrast, urinary 1. 5AG levels and NAG activity were significantly increased in STZ-induced diabetic rats. Urinary NAG activity also returned to the control levels after insulin treatment. These results indicate that high serum glucose levels may influence GAA synthesis renal tubular epithelial cells in diabetes. The measurement of GAA is a useful indicator for renal tubular dysfunction in the early phase of diabetes mellitus.