Hostname: page-component-7bb8b95d7b-fmk2r Total loading time: 0 Render date: 2024-10-04T16:35:59.019Z Has data issue: false hasContentIssue false
  • English
  • Français

Effects of litter size and subsequent gold-thioglucose-induced obesity on adipose tissue weight, distribution and cellularity in male and female mice: an age study

Published online by Cambridge University Press:  09 March 2007

Jennifer L. Roberts ,
Frances M. Whittington  and
Michael Enser
Jennifer L. Roberts
Affiliation:
AFRC Institute of Food Research, Bristol Laboratory, Langford, Bristol BS18 7DY
Frances M. Whittington
Affiliation:
AFRC Institute of Food Research, Bristol Laboratory, Langford, Bristol BS18 7DY
Michael Enser
Affiliation:
AFRC Institute of Food Research, Bristol Laboratory, Langford, Bristol BS18 7DY
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. Over- or undernutrition of newborn mice was caused by suckling in litters consisting initially of four or eighteen pups. After weaning mice were fed ad lib. At 13 weeks of age some mice from large litters received gold thioglucose (GTG: 600 mg/kg intraperitoneally) to induce hyperphagia, and mice were killed at 13, 19·5, 26, 39 and 52 weeks.

2. Total carcass lipid and the size and number of adipocytes in the inguinal subcutaneous, genital, perirenal and mesenteric depots were determined.

3. Mice, both male and female, raised in small litters were heavier and had more carcass fat at all ages than mice raised in large litters. After GTG-treatment mice from large litters were heavier and fatter than mice raised in small litters.

4. Fat distribution between the depots was related to carcass lipid content and not to treatment. The order of depot development was subcutaneous, parametrial, perirenal and mesenteric in females and epididymal, subcutaneous, perirenal and mesenteric in males. At 13 weeks the depots in males were more developed than those in females.

5. Litter size had no effect on adipocyte volume in female mice at 13 weeks but by 52 weeks small-litter mice had larger cells in all depots and more cells in the parametrial and perirenal depots.

6. Male mice from small litters had bigger cells at 13 weeks in all depots compared with males from large litters but by 52 weeks no significant differences remained. Greater numbers of cells were present only in the perirenal and mesenteric depots of small-litter males at some ages.

7. Depots of GTG-treated large-litter female mice had larger cells than those of small-litter females, while a similar number of cells was found by 52 weeks in all but the perirenal depot, which had significantly more cells.

8. GTG treatment of male mice from large litters also caused bigger cells than in small-litter mice, and an increased depot cell number at earlier ages in all but the epididymal depot. By 52 weeks cell numbers were similar in depots from small-litter and GTG-treated large-litter mice, except for the epididymal depot from the latter which had fewer cells.

9. Increases in cell numbers with age in different depots occurred independently of existing cell mean volume and even of tissue growth, suggesting the presence of an in-built chronology, at least in older mice.

10. We suppose that the differences in response to the level of preweaning nutrition in males and females result from a greater effect on the hypothalamic appetite centre in the latter. Whereas the cellular changes in large-litter males occur in the late-developing depots and are reversed naturally with time, those in the large-litter females are more extensive and require induction of hyperphagia for reversal.

Type
Research Article
Information
British Journal of Nutrition , Volume 59 , Issue 3 , May 1988 , pp. 519 - 533
Copyright
Copyright © The Nutrition Society 1988

References

Aubert, R., Suquet, J. P. & Lemonnier, D. (1971). Compte Rendu de I'Académie des Sciences, Paris, Série D 273, 2636–3638.Google Scholar
Bertrand, H. A., Masoro, E. J. & Yu, B. P. (1978). Science 201, 1234–1235.CrossRefGoogle Scholar
Björntorp, P., Karlsson, M. & Pettersson, P. (1982). Metabolism, Clinical and Experimental 31, 366–373.CrossRefGoogle Scholar
Eisen, E. J. & Leatherwood, J. M. (1978). Journal of Nutrition 108, 1652–1662.CrossRefGoogle Scholar
Enser, M., Roberts, J. & Whittington, F. M. (1985). British Journal of Nutrition 54, 645–654.CrossRefGoogle Scholar
Faust, I. M., Johnson, P. R. & Hirsch, J. (1980). Journal of Nutrition 110, 2027–2034.CrossRefGoogle Scholar
Faust, I. M., Johnson, P. R., Stern, J. S. & Hirsch, J. (1978). American Journal of Physiology 235, E279–E286.Google Scholar
Greenwood, M. R. C. & Hirsch, J. (1974). Journal of Lipid Research 15, 474–483.CrossRefGoogle Scholar
Gurr, M. I. & Kirtland, J. (1978). International Journal of Obesity 2, 401–425.Google Scholar
Hausberger, F. X. & Volz, J. E. (1984). Physiology and Behaviour 33, 81–87.CrossRefGoogle Scholar
Hausman, G. J. (1985). In New Perspectives in Adipose Tissue: Structure and Function, pp. 1–21 [Cryer, A. and Van, R. L. R., editors]. London: Butterworths.Google Scholar
Johnson, P. R. & Hirsch, J. (1972). Journal of Lipid Research 13, 2–11.CrossRefGoogle Scholar
Knittle, J. L. & Hirsch, J. (1968). Journal of Clinical Investigation 47, 2091–2098.CrossRefGoogle Scholar
Kral, J. G. (1976). American Journal of Physiology 231, 1090–1096.CrossRefGoogle Scholar
Lemonnier, D. (1972). Journal of Clinical Investigation 51, 2907–2915.CrossRefGoogle Scholar
McCance, R. A. (1976). Proceedings of the Nutrition Society 35, 309–313.CrossRefGoogle Scholar
Martin, R. J. (1974). Growth 38, 465–476.Google ScholarPubMed
Miller, W. H., Faust, I. M. & Hirsch, J. (1984). Journal of Lipid Research 25, 336–347.CrossRefGoogle Scholar
Reyne, Y., Teyssier, J., Nouguès, J. & Tébibal, S. (1985). Journal of Lipid Research 26, 1036–1046.CrossRefGoogle Scholar
Robelin, J. (1981). Journal of Lipid Research 22, 452–457.CrossRefGoogle Scholar
Sjöström, L., Björntorp, P. & Vrana, J. (1971). Journal of Lipid Research 12, 521–530.CrossRefGoogle Scholar
Stiles, J. W., Francendese, A. & Masoro, E. J. (1975). American Journal of Physiology 229, 1561–1568.CrossRefGoogle Scholar
Wise, A. (1975). Nutrition and Metabolism 19, 291–298.CrossRefGoogle Scholar