Activities of some regulatory enzymes of carbohydrate metabolism in the liver of rats fed a histidine-excess diet.

1. Glycogen is accumulated in the liver of rats given a histidine-excess diet. 2. In order to know the regulatory point, the activities of eight hepatic key enzymes in the carbohydrate metabolism were measured after feeding either a basal or a histidine-excess diet for 0, 3 and 7 days. 3. The active glycogen synthase level was about 2.6- and 3.0-fold higher after feeding for 3 and 7 days, respectively, but the total activity of this enzyme was not affected after feeding for 3 days and was increased after feeding for 7 days. 4. The active glycogen phosphorylase, glucose 6-phosphatase and pyruvate kinase activities were significantly decreased, and fructose 1,6-bisphosphatase activity was increased on a histidine-excess diet for 3 days. 5. Thus, of these enzymatic changes, mainly the enhancement of active glycogen synthase might lead to the substantial accumulation of hepatic glycogen. 6. The in vivo incorporation of radioactive glucose into liver glycogen was stimulated in rats given a histidine-excess diet.

The effect of a histidine-excess diet on cholesterol synthesis and degradation in rats.

Feeding a diet high in excess histidine (5% L-histidine) resulted in hypercholesterolemia and enlargement of the liver in rats. To clarify the mechanism of the hypercholesterolemia, cholesterol synthesis and degradation were followed. We found that hepatic 3-hydroxy-3-methylglutaryl-coenzyme A reductase activity in histidine-excess diet rats was significantly higher than in rats fed a basal diet. Incorporation of [3H] water into cholesterol of liver slices from rats fed the histidine-excess diet was higher than incorporation into liver slices from rats fed the basal diet (expressed per liver per 100 g body weight). In vivo incorporation of [3H] water into hepatic cholesterol was also higher, but the incorporation into cholesterol of the small intestine was lower in histidine-fed rats than in rats fed the basal diet (expressed per liver per 100 g body weight). Hepatic cholesterol 7 alpha-hydroxylase activity was similar in both groups. The data suggest that the hypercholesterolemia caused by histidine-excess diet appears to be due to the stimulation of cholesterol synthesis in the liver.

Effect of dietary excess-histidine on fructose 1,6-bisphosphatase and 6-phosphofructokinase activities, and activation of fructose 1,6-bisphosphatase by basic amino acids in rat liver.

1. Dietary excess histidine caused an increase in the total activity of fructose 1,6-bisphosphatase, and a decrease in 6-phosphofructokinase in the liver. 2. The hepatic concentrations of free histidine and lysine were higher in rats fed a histidine-excess diet. 3. The addition of histidine, lysine or arginine to the assay mixture for fructose 1,6-bisphosphatase resulted in a significant increase in its activity. The 6-phosphofructokinase activity in the liver was not enhanced by the addition of histidine to the assay mixture.

Fatty liver induced by the addition of excess cystine to a soy-bean protein diet in rats.

1. The effects of excess cystine added to diets with casein, egg protein, soya-bean protein and wheat gluten as protein source on liver and serum lipids of rats were compared. 2. The addition of excess cystine to a soya-bean protein diet produced lipid accumulation in the liver. 3. The addition of excess cystine to casein, egg protein and soya-bean protein diets, but not a wheat gluten diet, increased serum cholesterol.