Dietary sources of nucleotides may be conditionally essential nutrients. Rapidly growing tissues such as the intestinal epithelium and lymphoid cells lack significant capacity for de novo synthesis of nucleotides and require exogenous sources of purine and pyrimidine bases. Dietary purines are not significantly incorporated into hepatic nucleic acids, but pyrimidines are. Both are taken up by intestinal cells with excess purines converted to uric acid. Nucleotides are important for normal development, maturation and repair of the gastrointestinal tract. Human milk is the best source of nucleotides for young infants because cow's milk is lacking in nucleotide content. It is likely that infant formulas should have sources of nucleotides added to more closely duplicate human milk and provide these substrates for maximal intestinal development and repair.
It has become a common practice to supplement human milk with a variety of additives to improve the nutritive content of the feeding for the premature infant. Twenty-two freshly frozen human milk samples were measured for lysozyme activity, total IgA, and specific IgA to Escherichia coli serotypes 01, 04, and 06. One mL aliquots were mixed with the following: 1 mL of Similac, Similac Special Care, Enfamil, Enfamil Premature Formula, and sterile water; 33 mL of Poly-Vi-Sol, 33 mg of Moducal, and 38 mg of breast-milk fortifier, and then reanalyzed. Significant decreases (41% to 74%) in lysozyme activity were seen with the addition of all formulas; breast-milk fortifier reduced activity by 19%, while no differences were seen with Moducal, sterile water, or Poly-Vi-Sol. No differences were seen in total IgA content, but some decreases were seen in specific IgA to E. coli serotypes 04 and 06. E. coli growth was determined after 3 1/2 hours of incubation at 37 degrees C after mixing. All cow-milk formulas enhanced E. coli growth; soy formulas and other additives preserved inhibition of bacterial growth. Nutritional additives can impair anti-infective properties of human milk, and such interplay should be considered in the decision on the feeding regimen of premature infants.
We have tested the effectiveness of a commercial starch blocker on the digestion and absorption of dietary carbohydrates in six normal, healthy volunteers. The effectiveness of the starch blocker to attenuate or block the digestion of carbohydrate was assessed against a placebo by the measurement of end tidal breath hydrogen, plasma glucose, and insulin responses to a constant test meal. There were no significant differences in breath hydrogen, or plasma glucose and insulin responses. In vitro enzyme inhibition studies assessed the ability of the brush border enzyme maltase/glucoamylase to degrade starch in the presence of the starch blockers. A highly purified solution of rat and human maltase/glucoamylase was capable of degrading a starch solution, while 40 mM Tris-HCl (a known maltase/glucoamylase inhibitor) completely abolished the enzyme activity. These data challenge the claims that starch blocker preparations are effective in reducing or attenuating the absorption of carbohydrates or calories from a mixed meal. The ineffectiveness in vivo could be explained, in part, by the ability of the brush border enzyme maltase/glucoamylase to hydrolyze starch in the presence of starch blockers.
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