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Glycine has been used for many years as an orally administered test substance in the study of intestinal absorption. Most authors have utilized a technique measuring the total amino acid nitrogen of the blood at intervals after an oral dose of glycine, with the assumption that increases reflect the amount of glycine absorbed. Althausen, Doig, Uyeyama, and Weiden (1) have demonstrated the validity of this technique, but nevertheless concluded that absorptive tests for proteins and fats generally indicate greater impairment of absorption than do nutritional balance studies (2). There have been conflicting reports concerning the absorption of glycine in patients with sprue, although recent work suggests impaired absorption of virtually every normally absorbable substance , including sodium chloride (3). In 1935, Heath and Fullerton (4) noted similar curves of blood amino acid nitrogen after either oral or intravenous administration of glycine to patients with impaired absorption. They noted that about 75 per cent of an injected dose of glycine disappeared from the blood within four or five minutes. They concluded that glycine is without value in studying the absorptive capacity of the intestine. However, Erf and Rhoads (5) in 1940 presented evidence suggesting that glycine is absorbed from the gastrointestinal tract more slowly in patients with sprue or pernicious anemia than in normal subjects. Evidence of this abnormality was not demonstrable in the same patients after remission was induced with liver extract. Drew, Dixon, and Samuel (6) found satisfactory absorption of glycine in five patients with sprue in a convalescent state. In the investigations which form the basis of this repQrt chemical determinations of glycine and serine were carried out, in addition to the usual total amino acid nitrogen determination, in plasma from normal subjects and patients with sprue. This procedure was undertaken because of the role of folic acid in the conversion of glycine to serine and because of presumptive evidence that tropical sprue patients are deficient in this vitamin. The belief that such patients may be deficient in folic acid stems from observations that: 1) they show prompt clinical improvement with the sole addition of folic acid to a protein-poor, vitamin-deficient diet (7), and 2) there is a greatly diminished urinary excretion of folic acid by sprue patients (8). Das Gupta, Chatterjea, and Basu (9) believe that nutritional macrocytic anemia, sometimes considered as synonymous with sprue, results primarily from a deficiency of folic acid. It was postulated at …

THE ABSORPTION OF GLYCINE AND ITS CONVERSION TO SERINE IN PATIENTS WITH SPRUE