Abstract
The purpose of the present study was to determine whether the regulation of urea synthesis was mediated through the activation of N-acetylglutamate synthesis by arginine and whether the concentration of glutamate or activity of N-acetylglutamate synthetase might control N-acetylglutamate concentration when the thyroid status was manipulated. Three groups of rats were given 6-propyl-2-thiouracil (PTU, thyroid inhibitor) without triiodothyronine (T3) treatment, treated with PTU + T3 or treated with neither PTU nor T3 (control). Urinary excretion of urea, liver concentration of N-acetylglutamate and plasma concentration of arginine in rats given PTU + T3 were significantly lower than in rats given PTU alone. Liver concentration of N-acetyl-glutamate was correlated with plasma concentration of arginine (r = 0.842, P < 0.001). The activity of N-acetylglutamate synthetase and glutamate concentration in liver of the PTU + T3-treated group were significantly higher than in the group treated with PTU alone. Arginine administration (0.5 mmol/100 g body wt) elevated the liver concentration of N-acetylglutamate in all three groups. The results suggest that the greater concentration of arginine in the hypothyroid (PTU alone) rats is likely to increase the N-acetylglutamate concentration and stimulate urea synthesis.
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