The purpose of this study was to determine whether the quantity of dietary protein affects the rate of brain protein synthesis in aged rats. Experiments were conducted on three groups of 30-wk-old rats fed diets containing 0, 5 or 20 g casein/100 g for 10 d. The fractional rates of protein synthesis in brain, liver and kidney declined with a decrease in quantity of dietary protein. In brain, liver and kidney, RNA activity [g protein synthesized/(g RNA.d)] was significantly correlated with the fractional rate of protein synthesis. The RNA concentration (mg RNA/g protein) was not related to the fractional rate of protein synthesis in any organ. The results suggest that the rate of protein synthesis in the brain declines with a decrease in quantity of dietary protein in aged rats, and that RNA activity is at least partly related to the fractional rate of brain protein synthesis.

No abstract

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.

No abstract