Carbohydrate metabolism in birds. The site of the biochemical lesion in avian polyneuritis

Abstract

Recent work has defined a lowered power of oxygen uptake in certain parts of the pigeon’s brain in glucose-phosphate Ringer (Gavrilescu and Peters, 1931). The partial restoration of oxygen uptake which takes place upon addition of small amounts of vitamin B 1 concentrates, excluded lowered substrates alone as the cause of the effect. This could have been excluded upon other grounds, as several observers (Loebel, 1925; Meyerhof and Lohmann, 1926) have shown that lactate will prolong the oxygen uptake of brain tissue, and it is known that the avitaminous brain has more lactate than the normal. Since therefore the abnormality is concerned with the enzyme systems, it remains to be shown whether the effect is general, as would be expected from much of the previous literature upon the subject (see references in previous papers), or whether it is confined to an enzyme system for special substrates. In the latter case the vitamin would be concerned with one substrate and hence one phase of metabolism; in the former it would perhaps form part of the respiratory enzyme system (Warburg, 1928; Keilin, 1929). Holmes (1930) and Krebs (1931) have given reasons for the belief that glucose oxidation in brain proceeds via lactic acid, as the metabolism is disconnected between glucose-lactate stages in presence of fluoride or iodoacetic acid. A lesion affecting the intermediary metabolism is disconnected between the glucose-lactate stages in presence of fluoride or iodoacetic acid. A lesion affecting the intermediary metabolism of carbohydrate might be confined to glucose and lactate and not found with succinate (Quastel and Wheatley, 1931). Since the matter seemed crucial, we have compared the oxygen uptakes of normal and avitaminous brains in the presence of these three substrates, succinate being regarded as typical of another system. Since cyanide inhibits the uptake of oxygen for all three substrates, any difference in their behaviour in avitaminosis indicates that the vitamin acts specifically and not upon the indophenol oxidase. Our results show that a tissue may behave normally to succinate and yet abnormally to lactate, and are therefore consistent with the view that vitamin B 1 deficiency is connected essentially with the intermediary metabolism of carbohydrate.