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Growth and development of rats artificially reared on different milk-substitutes

Published online by Cambridge University Press:  09 March 2007

J. L. Smart ,
D. N. Stephens ,
J. Tonkiss ,
N. S. Auestad  and
J. Edmond
J. L. Smart
Affiliation:
Department of Child HealthThe Medical School, Oxford Road, Manchester M13 9PT
D. N. Stephens
Affiliation:
Department of Child HealthThe Medical School, Oxford Road, Manchester M13 9PT
J. Tonkiss
Affiliation:
Department of Child HealthThe Medical School, Oxford Road, Manchester M13 9PT
N. S. Auestad
Affiliation:
Department of Biological Chemistry and Mental Retardation Research Center, UCLA School of Medicine, Center for the Health Sciences, Los Angeles, California 90024, USA
J. Edmond
Affiliation:
Department of Biological Chemistry and Mental Retardation Research Center, UCLA School of Medicine, Center for the Health Sciences, Los Angeles, California 90024, USA
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Abstract

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1. Rat pups were artificially reared (AR) from postnatal day 4 or 5 till day 20 or 21, by fitting them with gastric cannulas through which milk-substitutes could be infused automatically.

2. Three milk-substitutes were compared: milk M, the usual diet for AR studies, which was somewhat low in protein and very high in carbohydrate; milk A, which resembled rats' milk much more closely in composition; and milk isoM, which was based on the high-energy milk M but was made isoenergetic with milk A. Pups given these diets were termet ARM, ARA and ARisoM respectively. Siblings of the AR rats were left with their mothers to form a mother-reared (MR) control group. Rats were autopsied at 20 or 21 d.

3. Growth in body-weight of all groups of AR pups lagged behind that of their MR siblings for about the first week of AR, but the ARM group showed complete catch-up and the ARA group partial catch-up in body-weight during the second week. ARisoM rats were growth-retarded throughout.

4. Inspection of organ weights expressed relative to body-weight revealed disturbances of organ growth in all AR groups compared with MR animals. ARM rats showed excessive epididymal fat pad and liver weights, but deficits in gastrocnemius muscle, heart and adrenal weights. In contrast, ARA rats usually displayed increased spleen and stomach weights, but lower weight of interscapular brown adipose tissue. ARisoM rats had high brain, liver and stomach weights and low muscle and spleen weights relative to body-weight. All AR groups had elongated small intestines.

5. Hence the patterns of abnormal organ growth differed between groups. Those shown by the ARM and ARisoM groups seemed the more seriously abnormal. The diet approximating the composition of rats' milk (milk A) appears, as intended, to be an improved milk-substitute.

Type
Papers of direct relevance to Clinical and Human Nutririon
Information
British Journal of Nutrition , Volume 52 , Issue 2 , September 1984 , pp. 227 - 237
Copyright
Copyright © The Nutrition Society 1984

References

Brown, E. G. & Sweet, A. Y. (1982). Pediatric Clinics of North America 29, 1149–1170.CrossRefGoogle Scholar
Diaz, J., Moore, E., Petracca, F., Schacher, J. & Stamper, C. (1981). Physiology and Behavior 27, 1103–1105.CrossRefGoogle Scholar
Diaz, J., Moore, E., Petracca, F., Schacher, J. & Stamper, C. (1982). Journal of Nutrition 112, 841–847.CrossRefGoogle Scholar
Diaz, J., Samson, H., Kessler, D., Stamper, C., Moore, E., Robisch, E. & Hodson, A. (1980). Pediatric Research 14, 595.Google Scholar
Dymza, H. A., Czajka, D. M. & Miller, S. A. (1964). Journal of Nutrition 84, 100–106.CrossRefGoogle Scholar
Glass, R. L., Troolin, H. A. & Jenness, R. (1967). Comparative Biochemistry and Physiology 22, 415–425.CrossRefGoogle Scholar
Grigor, M. R. & Warren, S. M. (1980). Biochemical Journal 188, 61–65.CrossRefGoogle Scholar
Hall, W. G. (1975). Science, New York 190, 1313–1315.CrossRefGoogle Scholar
Luckey, T. D., Mende, T. J. & Pleasants, J. (1954). Journal of Nutrition 54, 345–359.CrossRefGoogle Scholar
Messer, M., Thoman, E. B., Terrasa, A. G. & Dallman, P. R. (1969). Journal of Nutrition 98, 404–410.CrossRefGoogle Scholar
Miller, S. A. & Dymza, H. A. (1963). Science, New York 141, 517–518.CrossRefGoogle Scholar
Smart, J. L., Stephens, D. N. & Katz, H. B. (1983 a). British Journal of Nutrition 49, 497–506.CrossRefGoogle Scholar
Smart, J. L., Tonkiss, J., Stephens, D. N., Edmond, J. & Auestad, N. S. (1983 b). Proceedings of the Nutrition Society 42, 154A.Google Scholar
Smith, S., Watts, R. & Dils, R. (1968). Journal of Lipid Research 9, 52–57.CrossRefGoogle Scholar
Sonnenberg, N., Bergstrom, J. D., Ha, Y. H. & Edmond, J. (1982). Journal of Nutrition 112, 1506–1514.CrossRefGoogle Scholar
Winick, M. & Noble, A. (1966). Journal of Nutrition 89, 300–306.CrossRefGoogle Scholar