SummaryNitrogen metabolism was studied in three preterm infants (mean gestation 32 wk) by the method of consecutive metabolic balance. The absorption and retention of nitrogen from breast milk was measured, and protein turnover, synthesis, and breakdown were calculated from isotopic plateau of urinary urea and ammonia using an intermittent oral administration of "N-glycine. Weight gain and nitrogen retention were compared with the weight gain and nitrogen accumulated for a foetus of equivalent gestational age in utero.The average composition of the milk was 289 + 19 K J dl-' and 1.44 + 24 g protein dl-'. The intake of energy was 572 + 61 KJ kg-' day -' and of nitrogen 447 + 99 mg kg-' day-'. Stool output of nitrogen was 100 + 32 mg kg-' day-' giving an absorption of 348 + 78 mg kg-' day-', as urinary excretion was 91 + 17 mg kg-' day-' retained nitrogen was 256 2 71 mg kg-' day-', or 56% of intake.The specific weight gain was 15.6 5 2.6 g kg-' day-' and 53% of this comprised lean tissue (range 34 to 89%). In all but one study the postnatal retention of nitrogen fell far short of calculated in utero accumulation.The results of protein turnover were surprising. In six of the eight studies urinary urea failed to become enriched at all. Protein turnover calculated from the ammonia plateau was 1.94

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1. The evidence is accumulating to suggest that glycine, the simplest amino acid, is conditionally essential in man. Benzoic acid, by conjugation with glycine to form hippuric acid, is known to deplete the free glycine pool of the body. Glycine is one substrate for the enzyme glutathione synthase (EC 6.3.2.3) and in the inborn error of metabolism in which glutathione synthase function is defective, increased quantities of 5-oxoproline are excreted in the urine.2. An oral dose of 4-10 g sodium benzoate was given to six normal adults to deplete the metabolic pool of glycine, and the urinary excretion of 5-oxoproline was followed for 6 h. In five of the six, a significant increase in the urinary 5-oxoproline was seen within 3 h.3. These-findings show that 5-oxoprolinuria can result from limited glycine availability, and may provide a useful test for assessing glycine sufficiency in a range of physiological and pathological states.In human nutrition, glycine has generally been considered to be a nutritionally dispensable (non-essential) amino acid (Rose, 1957). There is an absolute requirement for dietary glycine in the chick, apparently to satisfy the demands of uric acid synthesis (Almquist et al. 1940). Moreover, when the rat is faced with either the physiological stress of growth (Griffith, 1929), or the pathological stress of injury or trauma (Sitren & Fisher, 1977), there is a narrow margin between the metabolic demand for glycine and the rate at which glycine can be formed or made available in the body. A marginal state of glycine availability is probably more common than has been appreciated in the past (Jackson, 1983). Recently, we presented evidence to show that glycine might behave as a conditionally essential amino acid in the preterm human infant (Jackson et al. 1981 ; Catzeflis et al.1985). Furthermore, Yu et al. (1985) have shown that in normal adults on a low-protein diet, glycine production in the body is insufficient to satisfy the normal metabolic demand. These findings suggest that glycine insufficiency might occur far more frequently, and be far more widespread than had been recognized (Christensen, 1986). It was for this reason that we had been looking for an index of glycine sufficiency in humans, that would be relatively simple to use in a range of clinical situations. The measurement of 5-oxoproline (50P), L-pyroglutamic acid, in urine possibly represents just such an index. In a range of physiological and pathological conditions in which we had predicted an excessive demand for glycine, we were able to demonstrate increased urinary excretion of 50P (Jackson et al. 1986).50P is a normal intermediate of the y-glutamyl cycle (Meister, 1983) and may be detected at low levels in the urine of healthy individuals. Excessive loss of 5 0 P in the urine, 5-oxoprolinuria (SOPuria), may be found in inborn errors of metabolism associated with either an increased production (glutathione synthase (EC 6.3.2.3) deficiency) or decreased utilization (5-oxoprolinase deficiency) of 50P by the body (Meister, 1...

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