Guanidinoacetic Acid (GAA) in Patients with Chronic Renal Failure (CRF) and Diabetes Mellitus (DM)

Tsubakihara, Yoshiharu; Iida, Nobutoshi; Yuasa, Shigekazu; Kawashima, Takashi; Nakanishi, Isao; Tomobuchi, M.; Yokogawa, Tomoko

doi:10.1007/978-1-4757-0752-6_30

Cited by 6 publications

(2 citation statements)

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“…Although there have been few papers showing the significance of pancreatic GAT in GAA metabolism in humans, the importance of GAA production in the kidney has been supported by some findings in the uremic state. Significant positive correla tions between Cr clearance and urinary GAA excretion, urinary GAA/GSA ratio and renal function, and signifi cant negative correlations between concentrations of serum GAA and BUN were reported in humans [10,13,22], Fur ther, it has been demonstrated that concentrations of plasma and intrarenal GAA are significantly lower in ex perimental C'RFanimals [II, 13,16], with significant negative correlations found between renal GAT activity and concen trations of BUN and significant positive correlations be tween renal GAT activity and serum concentrations of GAA in C'RF rabbits [11,13]. On the basis of these results, it is speculated that a decrease in renal GAT activity results in reduced production of GAA in CRF in vivo.…”

Section: Discussionmentioning

confidence: 94%

“…This substance plays an important role in muscle energy metabolism as a precursor of creatine (CR) and is synthesized from arginine (Arg) and glycine (Gly) by glycine amidinotransferase(GAT) mainly in the kidney and thereafter to C'R by GAA methyltransferase (GAA-MT) in the liver [7][8][9], It has been reported that in uremia, GAA production is reduced because of decreased GAT activity in the kidney, resulting in a lower concentration of serum GAA with a significant negative correlation with blood urea nitrogen (BUN) [10][11][12][13]. It has been suggested that GAA deficiency caused by the reduced production of GAA re sults in a CR deficiency in the uremic state [10][11][12][13][14][15]. Tsubakihara et al [12] reported that in chronic renal failure (CRF) rats, CR increased in each organ, while muscle strength and activity recovered when GAA was supplemented.…”

Section: Introductionmentioning

confidence: 99%

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Study on Impaired Metabolism of Guanidinoacetic Acid in Chronic Renal Failure Rabbits with Special Reference to Impaired Conversion of Arginine to Guanidinoacetic Acid

Kuroda

1993

Nephron

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Most chronic renal failure (CRF) patients show low serum concentrations of guanidinoacetic acid (GAA). In this study, the author investigated the impaired metabolism of GAA in CRF focusing on the transformation of arginine (Arg) to GAA by analyzing CRF rabbits using ¹⁴C-Arg. The CRF group which consisted of 6 CRF rabbits, was compared with 6 normal rabbits (normal group). Blood samples were obtained from each abdominal aorta after a bolus injection of 30 μCi of ¹⁴C-Arg into an ear vein of each rabbit. After the last sampling, the left kidney was obtained for measurement of renal glycine amidinotransferase (GAT) activity. In each blood sample, the concentrations of blood urea nitrogen (BUN), serum creatinine (Cr), GAA and Arg were measured. The radioactivity of serum ¹⁴C-GAA was measured with a liquid scintillation system. Δ¹⁴C-GAA was calculated as the difference between the ¹⁴C-GAA count and the Δ¹⁴C -background count. Serum concentrations of GAA and renal GAT activity were significantly lower in the CRF group as compared with the normal group. Significant negative correlations were found between the two groups for the following comparisons: serum concentrations of Cr and GAA, concentrations of BUN and renal GAT activity, and serum concentrations of Cr and renal GAT activity. There was a significant positive correlation in the two groups, between renal GAT activity and serum concentrations of GAA. The fact that the concentrations of neither GAA nor Arg changed significantly after the injection of ¹⁴C-Arg in either group suggested that the dosage of injected Arg is not sufficient to affect the transformation of Arg to GAA. After 5 min and at the following 5-min intervals, Δ¹⁴C-GAA was significantly lower in the CRF group than in the normal group. There was a positive correlation between Δ¹⁴C-GAA after 5 min and renal GAT activity. These results clearly show that renal GAT activity decreases with the progression of renal dysfunction, which directly causes a reduced transformation of Arg to GAA in the kidney, resulting in lower serum concentrations of GAA.

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