Hostname: page-component-745bb68f8f-mzp66 Total loading time: 0 Render date: 2025-01-24T11:14:13.150Z Has data issue: false hasContentIssue false
  • English
  • Français

Changes in adipose tissue of the rat due to early undernutrition followed by rehabilitation

3. Changes in cell replicafion studied with tritiated thymidhe

Published online by Cambridge University Press:  25 February 2008

Janet Kirtland  and
Patricia M. Harris
Janet Kirtland
Affiliation:
Nutrition Division, Unilever Research Laboratory, Colworth House, Sharnbrook, Beds MK44 ILQ and Department of Medicine, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ
Patricia M. Harris
Affiliation:
Nutrition Division, Unilever Research Laboratory, Colworth House, Sharnbrook, Beds MK44 ILQ and Department of Medicine, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ
Rights & Permissions [Opens in a new window]

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

1. Well-nourished rats were injected with tritiated thymidine at 15, 22, 28 or 84 d of age. At 1, 6, 11 and 16 d after injection animals from each group were killed, samples of adipose tissue were removed from two subcutanecus sites (abdominal and scapular) and separated, using collagenase (EC 3.4.24.3), into ‘fat cell’ and ‘stromal cell’ fractions. The specific (radio)activity of DNA isolated from each fraction was measured. The specific activity of DNA isolated from two ‘deep body’ sites (perirenal and epididymal) was measured only in the animals injected at 84 d of age.

2. Animals undernourished from birth up to 84 d of age were injected with tritiated thymidine at 22, 28 or 84 d of age. Animals were killed 1 and 11 d after injection, adipose tissue removed, and the specific activity of DNA measured. Other undernourished animals were rehabilitated from 84 to 107 d and injected at 91 d of age with tritiated thymidine. The animals were killed 1, 6, 11 and 16 d after injection, adipose tissue was removed from the subcutaneous and deep body sites and the specific activity of DNA determined as before.

3. In well-nourished animals fat cell replication had largely ceased by 12 weeks of age in the subcutaneous depots. There were differences between the various sites of adipose tissue regarding the period of hyperplastic growth, its timing or rate of replication or both.

4. In undernourished animals replication was slow in the subcutaneous depots compared with well-nourished animals of the same age. Rehabilitation from undernutrition stimulated replication which resulted in higher rates in all four depots examined compared with those in well-nourished animals.

5. The findings are discussed in relation to the concept of a finite period of hyperplasia for adipose tissue.

Type
Papers on direct relevance to Clinical and Human Nutrition
Information
British Journal of Nutrition , Volume 43 , Issue 1 , January 1980 , pp. 33 - 43
Copyright
Copyright © The Nutrition Society 1980

References

REFERENCES

Bertalanffy, F. D. & Lau, C. (1962). Inr. Rev. Cyrol. 13, 357.Google Scholar
Brook, C. G. D. (1975). Lancet i, 224.CrossRefGoogle Scholar
Burton, K. (1956). Biochem. J. 61, 315.CrossRefGoogle Scholar
Cleaver, J. E. (1967). Thymidine Metabolism and Cell Kinetics. Amsterdam: North-Holland.Google Scholar
DeRobertis, E. D. P., Nowinski, W. W. & Saez, F. A. (1965). Cell Biology. Philadelphia: W. Saunders & Co.Google Scholar
Greenwood, M. R. C. & Hirsch, J. (1974). J. Lipid Res. 15, 474.CrossRefGoogle Scholar
Gurr, M. I. & Kirtland, J. (1978). Inr. J. Obesity 2, 401.Google Scholar
Harris, P. M. (1980). Br. J. Nutr. 4, 27.CrossRefGoogle Scholar
Harris, P. M. & Widdowson, E. M. (1978). Br. J. Nutr. 39, 201.CrossRefGoogle Scholar
Hayes, T. M. & Lewis, B. M. (1975). Postgrud. med. J. 51, suppl. 1, 87.Google Scholar
Hirsch, J. & Batchelor, B. (1976). Endocr. Metab. 5, 299.Google Scholar
Hollenberg, C. H. & Vost, A. (1968). J. clin. Invest. 47, 2485.CrossRefGoogle Scholar
Jung, R. T., Gurr, M. I., Robinson, M. P. & James, W. P. T. (1978). Br. med. J. 2, 319.CrossRefGoogle Scholar
Kirtland, J. & Gurr, M. I. (1979). Inr. J. Obesiry 3, 15.Google Scholar
Lemmonier, D. (1972). J. clin. Invest. 51, 2907.CrossRefGoogle Scholar
Rodbell, M. (1964). J. biol. Chem. 239, 375.CrossRefGoogle Scholar
Widdowson, E. M. & Shaw, W. T. (1973). Lancet ii, 905.CrossRefGoogle Scholar
Winick, M. & Noble, A. (1966). J. Nutr. 89, 300.CrossRefGoogle Scholar
Zamenhof, S., Bursztyn, H., Rich, K. & Zamenhof, P. J. (1964). J. Neurochem. 11, 505.CrossRefGoogle Scholar