guanidinoacetic acid/糖尿病

We have already reported that renal glycine amidinotransferase (GAT) activity decreases in the course of renal damage, however, the inability of the kidney to synthesize guanidinoacetic acid (GAA) may be compensated by the pancreas in a more advanced stage of renal failure, and that in diabetes

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

We devised a clinical test of renal metabolism based on the synthesis of guanidinoacetic acid from citrulline in the proximal convoluted tubule. Intravenous administration of a citrulline/creatine solution to rats with modified levels of renal glycine amidinotransferase activity revealed a strong

Since urinary guanidinoacetic acid (GAA) derives from the kidneys, its detection is suggested to be associated with renal disease. We have been making a practice of investigating renal GAA production in diabetic patients, using a citrulline/creatine loading test. We noted a marked increase in

We present a method for the simultaneous determination of guanidinosuccinic acid (GSA) and guanidinoacetic acid (GAA) from urine by protein precipitation and liquid chromatography/tandem mass spectrometry. The chromatographic separation was performed using a cation exchange column with an elution