Nature of the stimulating action of insulin on lipogenesis from acetate in fasted rat liver.

In a previous communication we demonstrated that the ability to convert acetate to fatty acids is lowered in the liver of the fasted rat (1). A decreased rate of conversion was observed as early as 12 hours after food was withheld, and within 18 hours the liver had lost, to a great extent,, its ability to incorporate acetate into fatty acids. That this failure in hepatic lipogenesis was related to depressed glycolytic activity was suggested by several types of experiments. It was further pointed out that a reduction in circulating insulin could also have played a part in this defect. Indeed, it has been shown that the addition of insulin to the medium stimulates hepatic lipogenesis from acetate by surviving slices of liver (2, 3). The experiments reported here were designed to explore the interrelation of the actions of glucose and insulin upon hepatic lipogenesis.