Glucose and cycloheximide activated biosynthesis of phospholipids and, especially, of triacylglycerols involving 14C-acetate in rat liver tissue in vivo. Starvation did not affect the glycerolipid biosynthesis but decreased markedly the cholesterol production. In liver tissue of starved rats cycloheximide activated synthesis of glycerolipids and inhibited the cholesterol synthesis. Administration of glucose into the animals under conditions of their satiation augmented the fatty acid synthesis; the activating effect of cycloheximide was more distinct as compared with glucose. In satiated animals the most part of the label was incorporated into glycerolipid fatty acids after glucose and cycloheximide administration. Starvation inhibited synthesis of fatty acids with simultaneous activation of the glycerolipid glycerol production; cycloheximide activated still further the glyceroneogenesis. Both glucose and cycloheximide activated biosynthesis of palmitic and oleic acids of glycerolipids and inhibited the arachidonic acid synthesis. Similarity in the effect of glucose and cycloheximide on the glycerolipid biosynthesis might occur due to stimulation of glyceroneogenesis and to augmented production of alpha-glycerophosphate, which in turn increased the fatty acid esterification.