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The development of the weanling rat during nutritionally - induced growth retardation and during early rehabilitation

Published online by Cambridge University Press:  24 July 2007

P. A. McAnulty
Affiliation:
Department of Growth and Development, Institute of Child Health, Guilford Street, London, WCI N IEH
J. W. T. Dickerson
Affiliation:
Department of Biochemistry, University of Surrey, Guildford, Surrey
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Abstract

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1. Weanling (24-d-old) male rats were maintained at their body-weight for 1 month by restricting the intake of their normal diet. The animals were then rehabilitated for 0, 3, 7, 10 or 16 d. Control animals were given an unrestricted diet and some killed at the same body-weight as the experimental animals and others at the same age.

2. The forebrain, cerebellum, brain stem, heart, lungs, liver, spleen, kidneys, testes, and three sections of the alimentary tract were weighed, and DNA, RNA and protein contents were determined in the brain parts and liver.

3. During rehabilitation the weight of the body, corrected for the weight of the gut contents, showed a rapid gain between 7 and 10 d, which was synchronous with a rapid gain in weight of the testes.

4. The weight of the majority of organs relative to body-weight was maintained during both undernutrition and rehabilitation, the most marked exceptions being the stomach, which increased in relative weight during undernutrition, and maintained a high relative weight during rehabilitation, and the spleen, which lost weight during undernutrition, and on rehabilitation gained weight very rapidly to achieve a high relative weight.

5. The weight of the forebrain fell during undernutrition, due to a loss of water, and the weight of the brain stem rose. In the forebrain, DNA and the protein: DNA ratio were unchanged throughout, whereas a marked loss of RNA occurred during undernutrition, which was restored during rehabilitation.

6. The weight of the liver remained unchanged during undernutrition, despite increases in the amounts of DNA and protein. The amount of liver RNA decreased during undernutrition, but on rehabilitation showed an immediate and rapid increase. The variables measured in the liver were normal relative to body-weight, within 10 d of rehabilitation.

7. It is suggested that the growth occurring on rehabilitation is a balanced response to a single stimulus, partly mediated at the cellular level by RNA.

Type
General Nutrition
Copyright
Copyright © The Nutrition Society 1974

References

REFERENCES

Buchanan, T. A. S. & Pritchard, J. J. (1970). J. Anat. 107, 185.Google Scholar
Burton, K. (1956). Biochem. J. 62, 315.CrossRefGoogle Scholar
Caldarera, C. M., Barbiroli, B. & Moruzzi, G. (1965). Biochem. J. 97, 84.CrossRefGoogle Scholar
Cardell, R. R. jr (1971). Am. J. Anat. 131, 21.CrossRefGoogle Scholar
Cheek, D. B., Brasel, J. A. & Graystone, J. E. (1968). In Human Growth p. 306 [Cheek, D. B., editor]. Philadelphia: Lea and Febiger.Google Scholar
Clarke, M. F. & Smith, A. H. (1938). J. Nutr. 15, 245.CrossRefGoogle Scholar
Deane, H. W. (1944). Anat. Rec. 88, 39.CrossRefGoogle Scholar
Dickerson, J. W. T., Dobbing, J. & McCance, R. A. (1967). Proc. R. Soc. B 166, 396.Google Scholar
Dickerson, J. W. T., Hughes, P. C. R. & McAnulty, P. A. (1972). Br. J. Nutr. 27, 527.CrossRefGoogle Scholar
Dickerson, J. W. T. & McAnulty, P. A. (1972). Resuscitation 1, 61.CrossRefGoogle Scholar
Dickerson, J. W. T. & Walmsley, A. L. (1967). Brain 90, 897.CrossRefGoogle Scholar
Dickerson, J. W. T. & Widdowson, E. M. (1960). Proc. R. Soc. B 152, 207.Google Scholar
Dykstra, W. G. jr & Herbst, E. J. (1965). Science, N. Y. 149, 428.CrossRefGoogle Scholar
Giles, K. W. & Myers, A. (1965). Nature, Lond. 206, 93.CrossRefGoogle Scholar
Graystone, J. E. & Cheek, D. B. (1969). Pediat. Res. 3, 66.CrossRefGoogle Scholar
Løvtrup, S. & Swanson, V. L. (1958). Acta physiol. scand. 43, 51.CrossRefGoogle Scholar
Lowry, O. H., Rosebrough, N. J., Farr, A. L. & Randall, R. J, (1951). J. biol. Chem. 193, 265.CrossRefGoogle Scholar
McAnulty, P. A. & Dickerson, J. W. T. (1973). Pediat. Res. 7, 778.CrossRefGoogle Scholar
McMeekan, C. P. (1940). J. agric. Sci., Camb. 30, 276.CrossRefGoogle Scholar
Mendes, C. B. & Waterlow, J. C. (1958). Br. J. Nutr. 12, 74.CrossRefGoogle Scholar
Mugerwa, J. W. (1971). J. Path. 105, 105.CrossRefGoogle Scholar
Mulinos, M. G. & Pomerantz, L. (1940). J. Nutr. 19, 493.CrossRefGoogle Scholar
Munro, H. N. & Fleck, A. (1966). Meth. biochem. Analysts 14, 113.CrossRefGoogle Scholar
Osborne, T. B. & Mendel, L. B. (1915). J. biol. Chem. 23, 439.CrossRefGoogle Scholar
Osborne, T. B. & Mendel, L. B. (1916). Am. J. Physiol. 40, 16.CrossRefGoogle Scholar
Stekel, A. & Smith, N. J. (1970). Am. J. clin. Nutr. 23, 896.CrossRefGoogle Scholar
Trowell, H. C., Davies, J. N. P. & Dean, R. F. A. (1954). Kwashiorkor. London: Arnold.CrossRefGoogle ScholarPubMed
Widdowson, E. M. & McCance, R. A. (1960). Proc. R. Soc. B 152, 188.Google Scholar
Widdowscn, E. M. & McCance, R. A. (1963). Proc. R. Soc. B 158, 329.Google Scholar
Widdowson, E. M., Mavor, W. O. & McCance, R. A. (1964). J. Endocr. 29, 119.CrossRefGoogle Scholar
Winick, M. & Noble, A. (1966). J. Nutr. 89, 300.CrossRefGoogle Scholar
Winters, J. C., Smith, A. H. & Mendel, L. B. (1927). Am. J. Physiol. 80, 576.CrossRefGoogle Scholar