No abstract

IN a previous communication [Banerji, 1940] it was noted that the ingestion of a diet rich in fat caused a diminution in the excretion of bisulphite-binding substances in the urine of rats deficient in vitamin B1. It was hence thought worth while to investigate the effect of a high-protein diet on the excretion of these compounds by the deficient rats.

No abstract

It is now well established that vitamin B1 is concerned-in the metabolism of carbohydrate. Deficiency of the vitamin results in an accumulation in the blood of lactic acid [Callazo & Morelli, 1925] and of pyruvic acid [Thompson & Johnson, 1934; 1935; Platt & Lu, 1936]. It is now known that the pyrophosphate of vitamin B1 functions as a coenzyme in the decarboxylation of pyruvate [Lohmann & Schuster, 1937]. Studies on tissue respiration have shown that avitaminosis produces a diminished 02 uptake in many tissues, and Peters and his co-workers at Oxford were able to demonstrate that this diminished tissue respiration in polyneuritic animals, associated with an inability to oxidize pyruvate, may be rectified by the addition of vitamin B1 to the tissue respiring in vitro. They have called this phenomenon the 'catatorulin effect' [see Peters, 1936; 1940]. The role of vitamin B1 in carbohydrate metabolism has also been demonstrated by the fact that an increase in dietary' carbohydrate accentuates the symptoms of deficiency of the vitamin [e.g. Funk, 1914; Randoin & Simmonet, 1923]. It has also been shown recently that rats can thrive on a diet free from vitamin B1 if it contains no carbohydrate. Such animals grow well and do not develop such signs of deficiency as polyneuritis or bradcyeardia [see preceding papers of this series: Banerji, 1940; 1941]. The work described in this paper has arisen from the last-mentioned findings. The fact that it is possible for rats to survive in the absence of the vitamin with no signs of deficiency raises the question of the state of their tissues with regard to carbohydrate metabolism. This question may be put thus: does the defect in carbohydrate'oxidation, as shown for example by the catatorulin effect, persist in animals receiving no vitamin B1, even though they are free from symptoms of deficiency? The experiments to be described show that the defect does in fact persist aitid that deficient animals, irrespective of whether they develop symptoms, show a definite catatorulin effect.-It is clear that these results .are of significance in relation to the possible mode of action of the vitamin. This point will be discussed further after we have presented our results. EXPERIMENTAL Young rats weighing about 50 g. were fed on the folowing diets: (1) Standard basal diet (containing about 55 % sucrose). (2) High protein diet (sugar-free). (3) High fat diet (sugar-free). (4) Protein-fat diet (sugar-free). The detailed composition of the diets is shown in Table 1. Some of the animals received in addition supplements of vitamin B1, usually 0l,g. daily. (It has been shown that, with the standard basal diet, 8,ug. daily produce adequate growth [e.g. Yudkin, 1941].) Signs of deficiency developed only in those animals on the * Communicated to the Biochemical Society 21 March 1941 [Chem. and Ind. 60, 220].