Hostname: page-component-7479d7b7d-qs9v7 Total loading time: 0 Render date: 2024-07-12T11:35:17.913Z Has data issue: false hasContentIssue false
  • English
  • Français

Modification of glucocorticoid-induced changes in myofibrillar protein turnover in rats by protein and energy deficiency as assessed by urinary excretion of NT-methylhistidine

Published online by Cambridge University Press:  09 March 2007

F. M. Tomas ,
A. J. Murray  and
L. M. Jones
F. M. Tomas
Affiliation:
CSIRO Division of Human Nutrition, Kintore Avenue, Adelaide, South Australia 5000, Australia
A. J. Murray
Affiliation:
CSIRO Division of Human Nutrition, Kintore Avenue, Adelaide, South Australia 5000, Australia
L. M. Jones
Affiliation:
CSIRO Division of Human Nutrition, Kintore Avenue, Adelaide, South Australia 5000, Australia
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. The effects of differing degrees of experimental protein-energy malnutrition on the response of myofibrillar protein turnover rates to administration of corticosteroid has been studied in two experiments on rats. The basal control diet, offered ad lib. in each case, contained 40 g protein/kg, and other groups received diets containing 62.5, 95 or 220 g protein/kg at 0.67, 1 or 1.5 times the level of the control energy intake.

2. Daily administration of 25 or 30 mg corticosterone/kg body-weight after 18 d pre-feeding caused an increase in plasma protein, glucose and insulin concentrations, but a decrease in the corticosterone: insulin values. Liver size and protein content increased, as did the fractional excretion of dietary nitrogen as urea-N in all treated groups. However, whereas a fall in food intake and body-weight occurred in one experiment the reverse occurred in the other.

3. NT-Methylhistidine excretion was 12% lower for rats receiving 40 v. 220 g protein/kg diet and excretion was increased by only 57 v. 90% respectively, when the two groups of rats were given 30 mg corticosterone/kg per d. Rats which received 25 mg corticosterone/kg per d and up to 95 g protein/kg diet increased excretion of NT-methylhistidine by an average 35%.

4. The fractional degradation rate of myofibrillar protein (kd) was reduced by about 10% by the low-protein diet from 3.1 to 2.8%/d. During corticosterone treatment the increment in kd for rats on this diet was only 60% of that for rats receiving the 220 g protein/kg diet, i.e. an increase of 1.8 v. 3.0%/d. Energy restriction further reduced kd during low-protein intake but did not affect the response to the corticosterone. Variations in dietary protein from 40 to 95 g/kg had little effect on the increase in kd during steroid treatment. The effect of corticosterone on calculated synthesis rates (kg) differed markedly between experiments. While kg fell by 50–65% in rats which lost weight on treatment, it rose by up to 60% in rats where carcass non-collagen-protein accretion remained unchanged or increased, despite an increase in kd

5. Protein deficiency decreases the catabolic response to glucocorticoid, but the net metabolic response appears crucially dependent on changes in food intake or the stage of growth of the rat or both. A net anabolic response with increased fractional rates of myofibrillar protein breakdown, synthesis and accretion was observed in growing rats fed on relatively-low-protein diets and given 25 mg corticosterone/kg per d. This novel finding indicates that a particular role for cortisol in the adaptation to protein-energy malnutrition by humans should be ascribed only with caution.

Type
Papers of direct relevance to Clinical and Human Nutrition
Information
British Journal of Nutrition , Volume 51 , Issue 3 , May 1984 , pp. 323 - 337
Copyright
Copyright © The Nutrition Society 1984

References

REFERENCES

Bates, P. C. & Millward, D. J. (1981). Proceedings of the Nutrition Society 40, 89A.Google Scholar
Benville, P. E. & Tindle, R. C. (1970). Journal of Agricultural and Food Chemistry 18, 948–949.Google Scholar
Burini, R., Santidrian, S., Moreyra, M., Brown, P., Munro, H. N. & Young, V. R. (1981). Metabolism-Clinical and Experimental 30, 679–687.CrossRefGoogle Scholar
Coward, W. A. & Lunn, P. G. (1981). British Medical Bulletin 37, 19–24.CrossRefGoogle Scholar
Dorsey, T. E., McDonald, P. W. & Roels, O. A. (1977). Analytical Biochemistry 78, 156–164.CrossRefGoogle Scholar
Dunn, M. A., Houtz, S. K. & Hartsook, E. W. (1982). Journal of Nutrition 112, 1862–1875.CrossRefGoogle Scholar
Edozien, J. C., NiehausN., Mar N., Mar, M.-H.Makoui, T. Makoui, T. & Switzer, B. R. (1978). Journal of Nutrition 108, 1767–1776.CrossRefGoogle Scholar
Gallo, P. V. & Weinberg, J. (1981). Journal of Nutrition 111, 208–218.CrossRefGoogle Scholar
Goldberg, A. L., Tischler, M., DeMartino, G. & Griffin, G. (1980). Federation Proceedings 39, 31–36.Google Scholar
Golden, M. H. N. (1982). Lancet i, 1261–1265.CrossRefGoogle Scholar
Goodlad, G. A. J. & Munro, H. N. (1959). Biochemical Journal 73, 343–348.CrossRefGoogle Scholar
Griffin, E. E. & Wildenthal, K. (1978). American Journal of Physiology: Endocrinology and Metabolism 3, E306–E313.Google Scholar
Jaya Rao, K. S. (1974). Lancet i, 709–711.Google Scholar
Kelly, F. J. & Goldspink, D. F. (1982). Biochemical Journal 208, 147–151.CrossRefGoogle Scholar
Lowry, O. H., Rosebrough, N. J., Farr, A. L. & Randall, R. J. (1951). Journal of Biological Chemistry 193, 265–275.CrossRefGoogle Scholar
Lunn, P. G., Whitehead, R. G., Baker, B. A. & Austin, S. (1976). British Journal of Nutrition 36, 537–550.CrossRefGoogle Scholar
Lunn, P. G., Whitehead, R. G., Hay, R. W. & Baker, B. A. (1973). British Journal of Nutrition 29, 399–422.CrossRefGoogle Scholar
McGrath, J. A. & Goldspink, D. F. (1982). Biochemical Journal 206, 641–645.CrossRefGoogle Scholar
McNurlan, M. A. & Garlick, P. J. (1981). American Journal of Physiology: Endocrinology and Metabolism 4, E238–E245.Google Scholar
Millward, D. J. (1979). Proceedings of the Nutrition Society 38, 77–88.CrossRefGoogle Scholar
Millward, D. J., Garlick, P. J., Nnanyelugo, D. O. & Waterlow, J. C. (1976 a). Biochemical Journal 156, 185–188.CrossRefGoogle Scholar
Millward, D. J., Nnanyelugo, D. O., Bates, P. & Head, C. R. C. (1976 b). Proceedings of the Nutrition Society 35, 47A.CrossRefGoogle Scholar
Millward, D. J., Bates, P. C., Grimble, G. K., Brown, J. G., Nathan, M. & Rennie, M. J. (1980). Biochemical Journal 190, 225–228.CrossRefGoogle Scholar
Murray, A. J., Ballard, F. J. & Tomas, F. M. (1982). Analytical Biochemistry 116, 537–544.CrossRefGoogle Scholar
Nagabhushan, V. S. & NarasingaRao, B. S. Rao, B. S. (1978). American Journal of Clinical Nutrition 31, 1322–1327.CrossRefGoogle Scholar
Odedra, B., Bates, P. C., Nathan, M., Rennie, M. & Millward, D. J. (1980). Proceedings of the Nutrition Society 39, 82A.Google Scholar
Odedra, B. & Millward, D. J. (1982). Biochemical Journal 204, 663–672.CrossRefGoogle Scholar
Olusi, S. O., Orrell, D. H., Morris, P. M. & McFarlane, H. (1977). Clinica Chimica Acta 74, 261–269.CrossRefGoogle Scholar
Pennington, R. J. & Robinson, J. E. (1968). Enzymologia Biologica et Clinica 9, 175–182.CrossRefGoogle Scholar
Rannels, S. R. & Jefferson, L. S. (1980). American Journal of Physiology: Endocrinology and Metabolism 1, E564–E572.Google Scholar
Rikimaru, T., Yamamoto, S., Maeda, K. & Inoue, G. (1980). Journal of Nutritional Science and Vitaminology 26, 39–57.CrossRefGoogle Scholar
Rogers, Q. R. & Harper, A. E. (1965). Journal of Nutrition 87, 267–273.CrossRefGoogle Scholar
Santidrian, S., Moreyra, M., Munro, H. N. & Young, V. R. (1981). Metabolism—Clinical and Experimental 30, 798–804.CrossRefGoogle Scholar
Shoji, S. & Pennington, R. J. (1977). Molecular and Cellular Endocrinology 6, 159–169.CrossRefGoogle Scholar
Smith, I. F., Latham, M. C., Azubuike, J. A., Butler, W. R., Phillips, L. S., Pond, W. G. & Enwonwu, C. O. (1981). Proceedings of the Society for Experimental Biology and Medicine 167, 607–611.CrossRefGoogle Scholar
Technicon Instruments Co. Ltd (1965). Technicon Methodology Sheet N-11b. Basingstoke: Technicon Instruments Co. Ltd.Google Scholar
Technicon Instruments Co. Ltd (1967). Technicon Methodology Sheet N-1c. Basingstoke: Technicon Instruments Co. Ltd.Google Scholar
Tischler, M. E. (1981). Life Sciences 28, 2569–2576.CrossRefGoogle Scholar
Tomas, F. M. (1982). Biochemical Journal 208, 593–601.CrossRefGoogle Scholar
Tomas, F. M., Munro, H. N. & Young, V. R. (1979). Biochemical Journal 178, 139–146.CrossRefGoogle Scholar
Wassner, S. J. & Li, J. B. (1982). American Journal of Physiology: Endocrinology and Metabolism 6, E293–E297.Google Scholar
Waterlow, J. C., Garlick, P. J. & Millward, D. J. (1978). Protein Turnover in Mammalian Tissues and in the Whole Body. Amsterdam: North Holland.Google Scholar
Webster, D. (1977). Clinical Chemistry 23, 663–665.CrossRefGoogle Scholar
Whitehead, R. G. (1980). Proceedings of the Nutrition Society 39, 227–231.CrossRefGoogle Scholar
Whitehead, R. G. & Lunn, P. G. (1979). Proceedings of the Nutrition Society 38, 69–76.CrossRefGoogle Scholar