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.
SummaryThe purpose of this study was to find whether or not the ornithine transport into mitochondria regulated urea synthesis when the thyroid status is manipulated. Experiments were done on three groups of rats: given 6-propyl-2-thiouracil (PTU, a thyroid inhibitor) without tri iodothyronine (T3) treatment, treated with PTU+T3 or receiving neither PTU nor T3 (control). The urinary excretion of urea, liver concentration of ornithine and ornithine transport into isolated hepatic mitochondria in rats given PTU+T3 were significantly lower than in rats given PTU alone. Ornithine transport was significantly inhibited by the addition of lysine specifically. This response was achieved well within the physiological concentration of lysine. Compared with rats given PTU without T3 treatment, the liver concentration of lysine was significantly higher in rats treated with PTU+T3 and control rats. Ornithine transport into hepatic mitochondria was closely correlated with the excretion of urea. The results suggest that the greater ornithine transport in the hypothyroid (PTU alone) rats is likely to stimulate urea synthesis. A thyroid hor mone-induced increase in lysine concentration may be at least partly responsible for the changes in ornithine transport into mitochondria.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.