The relation of glucose oxidation to lipogenesis in mammary tissue.

Earlier studies with rat liver slices indicated that lipogenesis is dependent upon glucose utilization. Thus, liver slices prepared from fasted rats suffer from a lowered capacity to convert added acetate to fatty arids, and this defect in lipogenesis can be repaired by previous administration of glucose (1). hlore recently it was shown that an increase in fatty acid synthesis from acetate can be induced in the fasted liver by the addition of glucose to the incubation medium (2). Glycogen content has also been shown to be directly related to the amount of acetate carbon converted to fatty acids by liver slices (3). Because of its relatively high glycogen content, liver does not appear to be the tissue of choice for the study of this interrelation between carbohydrate and fat metabolism. Even though the amount of glycogen in liver can be lowered by fasting, this procedure impairs glucose utilization at an early phosphorylative stage (4). These difficulties with hepatic tissue can be circumvented by the use of mammary gland of the lactating ‘rat, a tissue that stores practically no glycogen, but which, in the presence of glucose, readily synthesizes fat (5, 6). The extremely low rate of endogenous glycolysis in isolated mammary gland has enabled us to study here the action of various added intcrmediates, per se, upon lipogenesis.