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The development of cold-induced thermogenesis and the structure of brown adipocyte mitochondria in genetically-obese (ob/ob) mice

Published online by Cambridge University Press:  09 March 2007

D. Hull
Affiliation:
Department of Child Health, E Floor, East Block, University Hospital, Nottingham NG7 2UH
J. Vinter
Affiliation:
Department of Child Health, E Floor, East Block, University Hospital, Nottingham NG7 2UH
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Abstract

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1. The onset of cold-induced thermogenesis was studied in a strain of mice which produced among their offspring genetically-obese (ob/ob) individuals. A thermogenic response was present in a majority by day 5 after birth.

2. The thermogenic response to cold was measured on days 5, 10 or 15 after birth, and the animals reared and the onset of obesity noted. The correlation between the subsequent development of obesity and a poor thermogenic response in early life was low.

3. A poor thermogenic response at day 15 was associated with the presence in brown adipocytes of mitochondria with disordered internal structures.

4. At day 42 both non-obese and obviously-obese mice showed a similar thermogenic response to moderate cold exposure.

5. It would seem that in this strain of mice disordered internal mitochondria1 structure in brown adipose tissue is associated with a poor thermogenic response to cold, but not invariably with the subsequent onset of obesity.

Type
Papers of direct relevance to Clinical and Human Nutrition
Copyright
Copyright © The Nutrition Society 1984

References

Alexander, G. (1975). British Medical Bulletin 31, 6267.CrossRefGoogle Scholar
Batt, R. A. L. & Hambi, M. (1982). International Journal of Obesity 6, 391397.Google Scholar
Davies, T. R. A. & Mayer, J. (1954). American Journal of Physiology 177, 222226.CrossRefGoogle Scholar
Elphick, M. C., Johnson, F., Davies, W. L. & Taylor, M. (1981). Medical and Biological Engineering and Computing 19, 110116.CrossRefGoogle Scholar
Grodums, E. I. (1977). Cell and Tissue Research 185, 231237.CrossRefGoogle Scholar
Hervey, G. R. & Tobin, G. (1983). Clinical Science 64, 718.CrossRefGoogle Scholar
Hogan, S. & Himms-Hagen, J. (1980). American Journal of Physiology 239, 301309.Google Scholar
Macdonald, I. A. & Stock, M. J. (1979). Nutrition and Metabolism 23, 250255.CrossRefGoogle Scholar
Rothwell, W. J. & Stock, M. J. (1983). Clinical Science 64, 1923.CrossRefGoogle Scholar
Stock, M. J. & Rothwell, W. J. (1979). Nature 281, 3135.Google Scholar
Suter, E. R. (1969 a). Journal of Ultrastructure Research 26, 216241.CrossRefGoogle Scholar
Suter, E. R. (1969 b). Laboratory Investigation 21, 246258.Google Scholar
Trayhurn, P., Thurlby, P. L. & James, W. P. T. (1977). Nature 266, 6061.CrossRefGoogle Scholar
Vinter, J., Hull, D. & Elphick, M. C. (1982). Biology of the Neonate 42, 145151.CrossRefGoogle Scholar