Interrelationship between Thiamine and Riboflavin in the Liver*

The possibility of an interrelationship between vitamins of the B group was first suggested by clinical observations. Scandinavian authors (l-3) have reported that treatment of multiple deficiencies with thiamine alone precipitated the appearance of lesions characteristic of nicotinic acid deficiency, and Sydenstricker (4) encountered the enhancement of certain signs of deficiency in pellagrins following treatment with nicotinic acid. These and other observations, taken as evidence of an interdependence between individual vit,amins of the B group, stimulated speculation as to whether the lack of one vitamin or an overdosage of an individual member of the vitamin B complex might derange the requirements for others (“vitamin balance”). Experimental data on an interdependence among the B vitamins are meager. Unna and Clark (5) were unable to show that excessive amounts of individual vitamins given to rats deficient in one or more factors of the vitamin B complex aggravate the manifestations of the specific deficiency. Klopp, Abels, and Rhoads (6) found a transitory increase in riboflavin excretion in men treated with large doses of thiamine. Prolonged administration of thiamine, however, failed to produce any clinical evidence of riboflavin deficiency. Sure and Ford (7) reported an increase in riboflavin excretion in the urine of thiamine-deficient rats. They suggested that thiamine deficiency, by affecting the utilization of riboflavin, may produce riboflavin deficiency in man. Ferrebee and Weissman (8), however, in studies on thiaminedeficient patients concluded that thiamine deficiency is not of clinical significance in the production of riboflavin deficiency. In thiaminedeficient rats, they observed changes in riboflavin metabolism only in the terminal stages of the deficiency, which were regarded as non-specific. Supplee, Jensen, Bender, and Kahlenberg (9) made the observation that the concentration of riboflavin in the liver increased temporarily following ingesting of food. This increase was not observed in thiamine-deficient and in pantothenic acid-deficient rats. Since the administration of these