AbstractEnzymes of the gluconeogenic pathway in animals adapt so as to exhibit increased activity during fasting, in diabetes, and following the administration of glucocorticoids. Many investigators have shown that these changes result from the synthesis of new enzyme protein rather than activation of latent forms of these enzymes. Glucocorticoids appear to induce the formation of several gluconeogenic enzymes, but the available evidence indicates this is a secondary rather than a primary response. Insulin appears to suppress formation of these enzymes, but experimental evidence indicates that insulinper seis not a repressor, nor is liver glycogen level. It is more likely that suppression of liver gluconeogenic enzymes by insulin is mediated by the latter's effect on availability of glucose to peripheral tissue. In liver and adipose tissue, enzymes that participate in lipogenesis (for example, citrate cleavage enzyme and malic enzyme) increase in activity following insulin administration. These enzymes are induced by available carbohydrate, and the induction is suppressed by fat.