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The sulphur-containing amino acid cysteine has been considered conditionally essential for premature and full-term newborn infants following Snyderman's work demonstrating improved N balance and growth when cysteine was provided (SNYDERMAN, 1971). In addition, cystathionase activity has been shown to be low during fetal development (GAULL, STURMAN and RAIHA, 1970). Thus, the formation of cysteine from methionine or serine would be limited. Because of this, the need to supplement TPN solutions used in the newborn infant with cysteine is generally recognised. However, some concern exists relative to its actual delivery to the tissues since cysteine is rapidly transported into cells (STEGINK, 1986). The addition of cysteine-containing dipeptides is likely to resolve this problem (STEGINK, 1986). Cysteine is necessary for protein synthesis, for glutathione formation and as a precursor for taurine.
The sulfonic amino acid taurine is not a component of structural proteins. It is the second most plentiful amino acid in human milk, and its formation requires an active transsulfuration pathway (GAULL et al., 1977). Due to the immaturity of this pathway in the newborn, as described above, it is also considered conditionally essential for the low birth weight infant. The adverse functional effect of taurine deficiency on retinal electrical responses to light have been well described (see GAULL and WRIGHT, 1986). More recently, the effect of taurine deficiency on auditory brains/em-evoked responses has been characterised in low birth weight infants given unsupplemented formula (GAULL and WRIGHT, 1986). Currently formulas for the premature infants are supplemented with 40 mg/dL, and parenteral solutions destined for this group of infants have also been supplemented. The need for taurine supplementation of the full-term formula-fed infant has not been established, yet most formulas have been supplemented to mimick human milk content. Other functional roles of taurine include its role in the conjugation of bile acids, its putative neurotransmitter role and an antioxidant effect on cell membranes, the latter influence being particularly important (see GAULL and WRIGHT, 1986).
Studies suggesting that the BCAAs can promote tissue anabolism (see WATERLOW, GARLICK and MILLWARD, 1978) led to considerable interest in the provision of BCAAs in TPN (FREUND, RYAN and FISCHER, 1978). In addition to any direct influence that the BCAAs might have on protein metabolism, there are several possibilities for indirect action. Since they transaminate in muscle, they can in theory act as precursors of muscle glutamine which, as discussed above, may exert anabolic effects. They could also influence brain tryptophan uptake and serotonin brain content and consequent neurological function as a result of competition between the BCAAs and aromatic amino acids for transport into the brain.
In practice, however, and notwithstanding a large number of attempts to make use of such interactions and improve outcome through nutritional support of patients with increased provision of the BCAAs parenterally or enterally, such attempts have generally been disappointing. Trials of their influence in patients with catabolic disease conducted by Fischer and colleagues, aimed at testing the hypothesis that these amino acids regulated protein balance in skeletal muscle, have also failed to provide consistent support (BOWER et al., 1986; FISCHER, 1991).
The possible influence of the BCAAs on AA transport into the brain, led to studies investigating the influence of the plasma aminogram and especially the balance between plasma BCAAs and the aromatic amino acids on the development of hepatic encephalopathy. Again, however, as reviewed by SHAW and LIEBER (1988), trials attempting to increase plasma BCAA levels with, for example, BCAA-enriched, low aromatic amino acid mixtures given parenterally to patients with acute hepatic encephalopathy, have been disappointing. Further examples of the use of the BCAAs are given in the chapter by Bistrian.
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