Liver homogenates were prepared from control, cold-fed and cold-fasted rats. Homogenates from control and cold-fed rats synthesized fatty acids to about the same extent. However, homogenates from cold-fasted rats converted far less acetate-1-C14 to fatty acids than homogenates from control and cold-fed rats. Previous studies showed that lipogenesis is depressed in liver slices from both cold-fed and cold-fasted rats. Probably the fact that lipogenesis is inhibited in the intact liver cells of cold-fed rats is not the result of reduced levels of fatty acid-synthesizing enzymes but is the result of an unfavorable cofactor environment; the evidence indicates that a low rate of TPNH generation via the hexose monophosphate pathway of carbohydrate metabolism causes the reduction in lipogenic activity. The failure in lipogenesis in the liver cells of the cold-fasted rat appears to result from quite a different cause than that of the cold-fed rat. The most likely reason for the low rate of lipogenesis in the liver of cold-fasted rats appears to be the loss of the fatty acid-synthesizing enzymes; however, the possibility that this lipogenic defect is related to the lack of a cofactor—as yet undiscovered— cannot be discounted.
