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Reasons why hypoalbuminaemia may or may not appear in protein-energy malnutrition

Published online by Cambridge University Press:  09 March 2007

W. A. Coward ,
R. G. Whitehead  and
P. G. Lunn
W. A. Coward
Affiliation:
Dunn Nutrition Unit, University of Cambridge and Medical Research Council, Cambridge CB4 1XJ
R. G. Whitehead
Affiliation:
Dunn Nutrition Unit, University of Cambridge and Medical Research Council, Cambridge CB4 1XJ
P. G. Lunn
Affiliation:
Dunn Nutrition Unit, University of Cambridge and Medical Research Council, Cambridge CB4 1XJ
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Abstract

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  1. 1. Investigations have been carried out in experimentally-malnourished rats in an attempt to explain the reasons for the development of the two main forms of protein-energy malnutrition in children, kwashiorkor and marasmus.

  2. 2. Isoenergetic diets with values for protein: energy (P:E) of 0.21 (control diet; C) 0.032 (low-protein diet; LP) and 0.005 (very-low-protein diet; VLP) were fed to groups of twenty-six rats either ad lib. or in restricted amounts from 5 weeks of age. Rats were killed at the start of the experiment and 1, 2 and 3 or 4 weeks later. Estimations were made of plasma albumin, insulin, corticosterone and amino acid concentrations and of the total protein content of the gastrocnemius muscles and liver.

  3. 3. Rats given diet LP ad lib. gained weight slowly and by week 1 plasma albumin concentration was slightly reduced. Rats given diet VLP ad lib. gradually lost weight and plasma albumin concentrations decreased continuously.

  4. 4. In contrast the major effect of dietary restriction during the first 2 weeks of the experiment was to maintain plasma albumin concentrations at normal values, irrespective of the diet given.

  5. 5. At later stages, however, when the ‘restricted’ animals had become very severely wasted, albumin concentrations decreased rapidly to values approaching those found in rats given diet VLP ad lib.

  6. 6. When diets LP and VLP were given ad lib. body protein was proportionally distributed in favour of muscle rather than liver. For ‘restricted’ rats the reverse was true, at least up to the time when plasma albumin concentration began to decrease.

  7. 7. Plasma corticosterone concentrations increased and insulin concentrations decreased when diets LP and VLP were fed in both an ad lib. and a ‘restricted’ regimen but the effects were significantly greater in the latter situation.

  8. 8. Ad lib. feeding of diets LP and VLP produced a distorted plasma amino acid pattern resembling that of kwashiorkor, but although dietary restriction resulted in a decrease in total amino acid concentration, the plasma concentration ratio, non-essential amino acids:essential amino acids was virtually unaffected.

  9. 9. It was concluded that whilst the lower the protein concentration in the diet the greater is the extent of hypoalbuminaemia which develops, dietary restriction with an increase in plasma glucocorticoid concentration and body-wasting can initially delay the development of the hypoalbuminaemia. However, in the final stages of wasting which ensue, low plasma albumin concentrations can appear because of a failure of the mechanisms which had earlier been able to preserve them at normal levels. It is possible that these two separate and distinct routes to hypoalbuminaemia observed in this study may have parallels in human situations in developing countries.

Type
Papers of direct relevance to Clinical and Human Nutrition
Information
British Journal of Nutrition , Volume 38 , Issue 1 , July 1977 , pp. 115 - 126
Copyright
Copyright © The Nutrition Society 1977

References

Annegers, J. F. (1973). Ecol. Fd Nutr. 2, 225.Google Scholar
Anthony, L. E. & Edozien, J. C. (1975). J. Nutr. 105, 631.Google Scholar
Arroyave, G. (1975). In Protein Calorie Malnutrition, p. 343 [Olson, R. E. editor]. New York and London: Academic Press.Google Scholar
Axton, J. H. M. (1975). Br. med. J. iii, 79.CrossRefGoogle Scholar
Brock., J. F. & Autret, M. (1952). FAO nutr. Stud. no. 8.Google Scholar
Coward, W. A. (1975). Br. J. Nutr. 34, 459.CrossRefGoogle Scholar
Coward, W. A. & Sawyer, M. B. (1974). Br. J. Nutr. 37, 127.Google Scholar
Dossetor, J. F. B. & Whittle, H. C. (1975). Br. med. J. ii, 592 Google Scholar
Edozien, J. C. (1968). Nature, Lond. 220, 917.Google Scholar
Enwonwu, C. O. & Sreebny, L. M. (1971). J. Nutr. 101, 501.CrossRefGoogle Scholar
Garlick, P. J., Millward, D. J., James, W. P. T., & Waterlow, J. C. (1975). Biochim, biophys Acta 414, 71.Google Scholar
Gopalan, C. (1968). In Calorie Deficiencies and Protein Deficiencies, p. 49 [McCance, R. A. and Widdowson, E. M., editors]. London: J. & A. Churchill.Google Scholar
Hales, C. N. & Randle, P. J. (1963). Biochem. J. 88, 137.Google Scholar
Kirsch, R., Saunders, S. S., Frith, L., Wicht, S. & Brock, J. F. (1969). S. Afr. med. J. 43, 125.Google Scholar
Lancet (1970). Lancet ii, 302.Google Scholar
Lowry, O. H., Rosebrough, N. J., Farr, A. L. & Randall, R. J. (1951). J. biol. Chem. 193, 265.Google Scholar
Lunn, P. G., Whitehead, R. G. & Baker, B. A. (1976). Br. J. Nutr. 36, 219.Google Scholar
Lunn, P. G., Whitehead, R. G., Baker, B. A. & Austin, S. (1976). Br. J. Nutr. 36, 537.Google Scholar
Lunn, P. G., Whitehead, R. G., Hay, R. W. & Baker, B. A. (1973). Br. J. Nutr. 29, 399.Google Scholar
McCance, R. A. & Widdowson, E. M. (1966). Lancet ii, 158.Google Scholar
Millward, D. J., Garlick, P. J., Nnanyelugo, D. O. & Waterlow, J. C. (1976). Biochem. J. 156, 185.Google Scholar
Munro, H. N. (1964). In Mammalian Protein Metabolism, Vol. 1, p. 381 [Munro, H. N. and Allison, J. B., editors]. New York and London: Academic Press.Google Scholar
Murphey, B. E. P. (1967). J. clin. Endocr. 27, 973.CrossRefGoogle Scholar
Northam, B. E. & Widdowson, G. M. (1967). Ass. Clin. Biochem. Tech. Bull. no. 11.Google Scholar
Philbrick, D. J. & Hill, D. C. (1974). Am. J. clin. Nutr. 27, 813.Google Scholar
Rothschild, M. A., Oratz, M., Mongelli., J., Fishman, L. & Schreiber, S. S. (1969). J. Nutr. 98, 395.Google Scholar
Scrimshaw, N. S. (1975 a). In Protein Calorie Malnutrition, p. 345 [Olson, R. E. editor]. New York and London: Academic Press.Google Scholar
Scrimshaw, N. S. (1975 b). In Protein Calorie Malnutrition, p. 353 [Olson, R. E. editor]. New York and London: Academic Press.Google Scholar
Technicon Instruments Co. Ltd. (1972). Technicon Clinical Method no. 509-72E. Basingstoke, Hants: Technicon Instruments Co. Ltd.Google Scholar
Waterlow, J. C. (1975). In Protein Calorie Malnutrition, p. 348 [Olson, R. E. editor]. New York and London: Academic Press.Google Scholar
Whitehead, R. G. (1971). Proceedings: 13th International Congress of Paediatrics, Vol. 2, pt 1: Nutrition and Gastroenterology, p. 231. Vienna: Wiener Medizinischen Akademie.Google Scholar
Whitehead., R. G. & Alleyne, G. A. O. (1972). Br. med. Bull. 28, 72.CrossRefGoogle Scholar