The injection of large amounts of glucosamine into either alligators or rats increased the plasma glucose level to a height as great as that found in severe diabetes. Galactosamine and N-acetylglucosamine were inactive in this respect. Since glucosamine was not found to increase plasma lactic acid in either the alligator or rat or to decrease liver glycogen in the rat, it did not appear to function as a glycogenolytic agent. The injection of glucose combined with amounts of glucosamine which were too small to cause hyperglycemia in either animal led to the development of a very much more marked hyperglycemia than when glucose alone was injected. The evidence indicated that glucosamine inhibited glucose utilization and hence it could be considered to be diabetogenic. Neither glucosamine nor galactosamine were utilized for energy to any great extent and both were excreted in the urine of the two species as rapidly as thiosulfate, an inert compound known to be eliminated at renal filtration rate. Glucosamine and galactosamine in very small doses constricted the pupils of the eyes of the alligator. This miotic response and the glucosamine-induced hyperglycemia were decreased by insulin injections. Insulin hastened the disappearance of glucosamine from the plasma of the alligator.