Abstract: Publisher Summary This chapter focuses on three devices: catabolite repression, transient repression, and catabolite inhibition, which regulate the utilization of many carbohydrates. Catabolite repression is a reduction in the rate of synthesis of certain enzymes, particularly those of degradative metabolism, in the presence of glucose or other readily metabolized carbon sources. Catabolite inhibition is a control exerted by glucose on enzyme activity rather than on enzyme formation, analogous to feedback inhibition in biosynthetic pathways. Catabolite repression influences many aspects of microbial growth and metabolism. In addition to the well known repressions of carbohydrate utilization and amino-acid degradation in bacteria and yeast, catabolite repression affects the formation of enzymes that function in the tricarboxylic acid cycle, glyoxylate cycle, fatty acid degradation, carbon dioxide fixation, and the respiratory chain. In higher organisms, catabolite repression has been observed in sugar cane, rats, and man. The question of whether catabolite repression acts to inhibit the transcription of DNA into m-RNA or to inhibit translation of messenger into protein has received conflicting answers. Catabolite repression is a control system that usually affects catabolic enzymes. If catabolite repression and transient repression are not mediated by the specific apo-repressor of each operon, there must be another protein that recognizes the low molecular-weight effector. The significance of a control mechanism, which influences the activity as opposed to the concentration of a carbohydrate-metabolizing enzyme is readily appreciated because bacteria have a limited ability to change enzyme concentrations.