Role of N-acetylglutamate turnover in urea synthesis by rats treated with the thyroid hormone.
We determined whether the synthesis and degradation of N-acetylglutamate would regulate urea synthesis when the thyroid status was manipulated. Experiments were done on three groups of rats, each being given 6-propyl-2-thiouracil (PTU, a thyroid inhibitor) without a triiodothyronine (T3) treatment, treated with PTU + T3, or receiving neither PTU nor T3 (control). The plasma concentration and urinary excretion of urea, the liver concentration of N-acetylglutamate, and the liver N-acetylglutamate synthesis in rats given PTU alone were each significantly higher than in the control rats. Compared with the control rats, the liver N-acetylglutamate degradation was significantly lower in those rats given PTU without the T3 treatment. Treatment of the PTU-treated rats with T3 reversed the effects of PTU to the values of the control rats. N-Acetylglutamate synthesis in the liver was closely correlated with the excretion of urea, and inverse correlation between the liver N-acetylglutamate degradation and urea excretion was found. These results suggest that the greater synthesis and lower degradation of N-acetylglutamate in the hypothyroid (PTU alone) rats would be likely to increase the hepatic concentration of this compound and stimulate urea synthesis.
Hayase
K
K
Department of Home Economics, Aichi University of Education, Japan.
Naganuma
Y
Y
Koie
M
M
Yoshida
A
A
D000818:Animals; D005971:Glutamates / Q000096:biosynthesis / Q000378:metabolism*; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D011441:Propylthiouracil / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013961:Thyroid Gland / Q000187:drug effects / Q000502:physiology; D014284:Triiodothyronine / Q000494:pharmacology*; D014508:Urea / Q000097:blood / Q000378:metabolism* / Q000652:urine
D005971:Glutamates; D014284:Triiodothyronine; D011441:Propylthiouracil; D014508:Urea; C016195:N-acetylglutamic acid