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The growth and development of rats given a low-protein diet

Published online by Cambridge University Press:  09 March 2007

J. W. T. Dickerson ,
P. C. R. Hughes  and
P. A. McAnulty
J. W. T. Dickerson
Affiliation:
Department of Biochemistry, University of Surrey, Guildford
P. C. R. Hughes
Affiliation:
Department of Growth and Development, Institute of Child Health, Guilford Street, London WC1 N1EH
P. A. McAnulty
Affiliation:
Department of Growth and Development, Institute of Child Health, Guilford Street, London WC1 N1EH
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Abstract

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1. Weanling (24-d-old) rats of a black and white hooded strain were allowed free access for 28 d to a diet containing 5% casein supplemented with methionine, and sucrose as the carbohydrate. Controls were fed on a 25% casein diet with a corresponding reduction in sucrose. Animals given the deficient diet were killed either at 52 d of age or after subsequent rehabilitation on the 25% casein diet when aged 140 d. These animals were compared with controls killed at these two ages and at the start of the experiment.

2. The skeletons were X-rayed, skeletal maturity was determined according to a scoring system, and various bones were measured. The forebrain and cerebellum were analysed for cholesterol and DNA and the brain stem for cholesterol only. The DNA content of the paired quadriceps muscles and the livers was also determined.

3. On the low-protein diet the body-weight rose by 7 g compared with the control value of 115 g. On rehabilitation, the body-weight of the previously malnourished group showed the expected growth spurt, but failed to attain that of the controls at 140 d.

4. With the exception of the pelvis width, all the bones grew a little during the period on the low-protein diet. After rehabilitation, the hind limb, pelvis, iliac and spine lengths and the bi-iliac width remained smaller than these measurements in the corresponding controls, whereas there was no difference in the length of the fore limb, width of the pelvis or in the bone maturity score.

5. The forebrains and cerebellums of the malnourished rats did not increase in weight, whereas some increase occurred in the brain stem. The concentration of cholesterol in the forebrains of the deficient animals was the same as that in controls of the same age, but on rehabilitation the concentration did not rise to the control value. The concentration of cholesterol in the cerebellum and brain stem of the deficient rats was lower than in controls of the same age but, whereas that in the cerebellum attained an almost normal level on rehabilitation, that in the brain stem remained significantly lower. The low-protein diet prevented the normal increase in cerebellum DNA and the amount remained low in the rehabilitated animals.

6. The experimental diet caused a complete cessation of growth of the quadriceps muscles, and even after rehabilitation they weighed less than their controls. The DNA content, however, was not significantly lower.

7. The low-protein diet did not permanently affect either the weight or DNA content of the liver.

Type
General Nutrition
Information
British Journal of Nutrition , Volume 27 , Issue 3 , May 1972 , pp. 527 - 536
Copyright
Copyright © The Nutrition Society 1972

References

Bruce, H. M. (1957). Stud. Fertil. 9, 90.Google Scholar
Burton, K. (1956). Biochem. J. 62, 315.Google Scholar
Dickerson, J. W. T. (1968). In Calorie Dejiciencies and Protein Deficiencies p.329 [McCance, R. A. and Widdowson, E. M., editors]. London: Churchill.Google Scholar
Dickerson, J. W. T., Dobbing, J. & McCance, R. A. (1967). Proc. R. Soc. B. 166, 396.Google Scholar
Dickerson, J. W. T. & Jarvis, J. (1970). Proc. Nutr. Soc. 29, 4A.Google Scholar
Dickerson, J. W. T. & McCance, R. A. (1960). Br. J. Nutr. 14, 331.Google Scholar
Dickerson, J. W. T. & Walmsley, A. W. (1967). Brain 90, 897.Google Scholar
Dobbing, J. (1964). Proc. R. Soc. B. 159, 503.Google Scholar
Dobbing, J. (1968). In Applied Neurochemistr. p.287 [Davison, A. N. and Dobbing, J., editors]. Oxford: Blackwell Scientific Publications.Google Scholar
Dobbing, J. & Widdowson, E. M. (1965). Brain 88, 357.CrossRefGoogle ScholarPubMed
Folch, J., Lees, M. & Stanley, G. H. S. (1957). J. biol. Chem. 226, 497.Google Scholar
Graystone, J. E. & Cheek, D. B. (1969). Pediat. Res. 3, 66.CrossRefGoogle Scholar
Hughes, P. C. R. & Tanner, J. M. (1970 a). J. Anat. 106, 349.Google Scholar
Hughes, P. C. R. & Tanner, J. M. (1970 b). J. Anat. 106, 371.Google Scholar
Kennedy, G. C. (1957–1958). J. Endow. 16, 9.CrossRefGoogle Scholar
Kissane, J. M. & Robbins, E. (1958). J. biol. Chem. 233, 184.Google Scholar
Leffler, H. H. (1959). Am. J. din. Path. 31, 310.Google Scholar
Widdowson, E. M. & McCance, R. A. (1960). Proc. R. Soc. B. 152, 188.mxGoogle Scholar
Winick, M. & Noble, A. (1966). J. Nutr. 89, 300.Google Scholar
Zamenhof, S., Bursztyn, H., Rich, K. & Zamenhof, P. J. (1965). J. Neurochem. 11, 505.CrossRefGoogle Scholar