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Protein Dynamics during Refeeding of Protein-Depleted Rats: Effects of Increasing Amino Acid Intake by TPN or Enteral Continuous Feeding^{1, 2,}

The Nutrition/Metabolism Laboratory, Cancer Research Institute, New England Deaconess Hospital/Harvard Medical School, Boston, MA 02215

The effect of increasing nitrogen intake with constant calorie supply was studied in protein-depleted rats. Animals were randomized into three paired groups to receive either total parenteral nutrition (TPN) or enteral (EF) isocaloric feedings (240 kcal · kg^-1 · day^-1) differing only in their amount of amino acids. The diets, composed of dextrose, a safflower oil emulsion and crystalline amino acids, were infused continuously for 5 days. Daily nitrogen intakes were for controls (EF, n = 7; TPN, n = 6) 0.25 g/kg; for groups 1 (EF, n = 7; TPN, n = 8) 1.4 g/kg and for groups 2 (EF, n = 7; TPN, n = 7) 2.5 g/kg. The rats in groups 1 and 2 obtained significant protein repletion in terms of body weight, nitrogen retention, liver protein and serum albumin regardless of the route of nutrient delivery. However, rats in groups 2 (higher nitrogen intake) presented a more rapid and greater recovery despite a reduction in nitrogen utilization. Whole-body leucine kinetics studied at the end of controlled feeding periods were similar for EF and TPN rats. However, increasing nitrogen intake (1 and 2) increased whole-body leucine flux and incorporation into protein resulting in a better balance, since leucine release from protein breakdown was comparable to controls. Liver protein fractional synthetic rates were reduced in EF while remaining at a high rate in TPN group 2 and still more elevated in TPN group 1, suggesting a preferential support of liver protein by enteral feeding or the effect of TPN as a nonphysiologic route.

KEY WORDS: • malnutrition • leucine kinetics

¹ Presented in part at the 7th Clinical Congress of The American Society for Parenteral and Enteral Nutrition, January, 1983, Washington, DC. Abstract published in J. Parent. Ent. Nutr. 6: 580, 1982.

² Supported in part by grants GM-24401 and GM-24206 awarded by the National Institute of General Medical Sciences, Department of Health and Human Services, and RR-05591 awarded by Research Resources Division of National Institutes of Health. A. Maiz was supported in part with a visiting research fellowship from the Pontificia Universidad Católica de Chile.

³ Reprint requests should be directed to: B. R. B., Cancer Research Institute, 194 Pilgrim Road, Boston, MA 02215. This is reprint No. 743 of the Cancer Research Institute, New England Deaconess Hospital.

Manuscript received 21 March 1983.