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The effect of underfeeding on the physiological response to food ingestion in normal weight women

Published online by Cambridge University Press:  09 March 2007

P. I. Mansell
Affiliation:
Department of Physiology and Pharmacology, Medical School, Queen's Medical Centre, Nottingham NG7 2UH
I. A. Macdonald
Affiliation:
Department of Physiology and Pharmacology, Medical School, Queen's Medical Centre, Nottingham NG7 2UH
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Abstract

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1. The thermogenic, cardiovascular and metabolic responses to the ingestion of a 30 kJ/kg body-weight test meal were studied in six normal weight, female subjects before and after a 7 d period of underfeeding at 60 kJ/ kg ideal body-weight per d.

2. With underfeeding there were decreases in body-weight, plasma insulin and 3,5,3'-triiodothyronine concentrations, resting metabolic rate and respiratory exchange ratio, with increased blood ketone levels. Baseline ‘arterialized’ venous plasma noradrenaline and adrenaline concentrations were not affected by underfeeding.

3. Ingestion of the test meal caused similar increases in heart rate and calf blood flow and changes in blood pressure in the fed and underfed states. There was a greater glycaemic response to the test meal in the underfed state compared with the fed state although the rise in plasma insulin concentration was similar and ketogenesis was suppressed. The increases in metabolic rate and plasma noradrenaline concentrations following the test meal were similar in the fed and underfed states.

4. Although the period of underfeeding in the present study led to considerable metabolic adaptation, and some alteration in physiological responses to ingestion of a test meal, there was no evidence that there were associated changes in sympathetic nervous system activation.

Type
Clinical and Human Nutrition Papers: Studies in Man
Copyright
Copyright © The Nutrition Society 1988

References

Acheson, K., Jequier, E. &, Wahren, J. (1983). Journal of Clinical Investigation 72, 981986.CrossRefGoogle Scholar
Acheson, K., Ravussin, E., Wahren, J. &, Jequier, E. (1984). Journal of Clinical Investigation 74, 15721580.CrossRefGoogle Scholar
Astrup, A., Bulow, J., Christensen, N. J., Madsen, J. &, Quaade, F. (1986). American Journal of Physiology 250, E226E229.Google Scholar
Chang, P. C., van der Krogt, J. A., Vermeij, P. &, van Brummelen, P. (1986). Hypertension 8, 801809.CrossRefGoogle Scholar
De Fronzo, R. A., Soman, V., Sherwin, R. W., Hendler, R. &, Felig, P. (1978). Journal of Clinical Investigation 62, 204213.CrossRefGoogle Scholar
Esler, M. (1982). Clinical Science 62, 247254.CrossRefGoogle Scholar
Fellows, I. W., Bennett, T. &, Macdonald, I. A. (1985). Clinical Science 69, 215222.CrossRefGoogle Scholar
Fellows, I. W. &, Macdonald, I. A. (1985). Clinical Physics and Physiological Measurement 6, 349355.CrossRefGoogle Scholar
Flatt, J. P. (1978). In Recent Advances in Obesity Research, pp. 211218 [Bray, G. A., editor]. London: Newman.Google Scholar
Jung, R. T., Shetty, P. S., Barrand, M., Callingham, B. A. &, James, W. P. T. (1979). British Medical Journal i, 1213.CrossRefGoogle Scholar
Jung, R. T., Shetty, P. S. &, James, W. P. T. (1980). Clinical Science 58, 183191.CrossRefGoogle Scholar
Landsberg, L. &, Young, J. B. (1985). In Neuroendocrine Perspectives, Vol. 4, pp. 191218 [MillerE. E., E. E.,Macleod, R.M. and Frohman, L. A., editors]. New York: Elsevier Science Publishers.Google Scholar
Lloyd, B., Burin, J., Smythe, P. &, Alberti, K. G. M. M. (1978). Clinical Chemistry 24, 17241729.CrossRefGoogle Scholar
Macdonald, I. A. &, Lake, D. M. (1985). Journal of Neuroscience Methods 13, 239248.CrossRefGoogle Scholar
McGuire, F., Heldman, J., Tobin, J., Andres, R. &, Berman, M. (1976). Journal of Applied Physiology 41, 565573.CrossRefGoogle Scholar
Metropolitan Life Insurance Company (1959). Statistical Bulletin 40, 1.Google Scholar
Morgan, J. B. (1984). International Journal of Obesity 8, 629640.Google Scholar
Qamar, M. F. &, Read, A. E. (1985). Quarterly Journal of Medicine 56, no. 220, 417419.Google Scholar
Rowe, J. W., Young, J. B., Minaker, K. L., Stevens, A. L., Pallotta, J. &, Landsberg, L. (1981). Diabetes 30, 219225.CrossRefGoogle Scholar
Schutz, Y., Golay, A., Felber, J.-P. &, Jequier, E. (1984). American Journal of Clinical Nutrition 39, 380387.Google Scholar
Schwartz, R. S., Halter, J. B. &, Bierman, E. L. (1983). Metabolism 32, 114117.CrossRefGoogle Scholar
Schwartz, R. S., Jaeger, L. F., Silberstein, S. &, Veith, R. C. (1987). International Journal of Obesity 11, 141149.Google Scholar
Shetty, P. S., Jung, R. T., James, W. P. T., Barrange, M. A. &, Callingham, B. A. (1981). Clinical Science 60, 519525.CrossRefGoogle Scholar
Stock, M. J. (1980). European Journal of Applied Physiology 43, 3540.CrossRefGoogle Scholar
Swaminathan, R., King, R. F. G. J., Holmfield, J., Swieck, R. A., Baker, M. &, Wales, J. K. (1985). American Journal of Clinical Nutrition 42, 177181.CrossRefGoogle Scholar
Webb, P. (1986). American Journal of Clinical Nutrition 44, 614619.CrossRefGoogle Scholar
Weir, J. B. de V. (1949). Journal of Physiology 109, 19.CrossRefGoogle Scholar
Welle, S. &, Campbell, R. G. (1983). American Journal of Clinical Nutrition 37, 8792.CrossRefGoogle Scholar
Welle, S., Lilavivat, U. &, Campbell, R. G. (1981). Metabolism 30, 953958.CrossRefGoogle Scholar
Whitney, R. J. (1953). Journal of Physiology 121, 127.CrossRefGoogle Scholar