Hostname: page-component-586b7cd67f-2brh9 Total loading time: 0 Render date: 2024-11-30T01:32:01.875Z Has data issue: false hasContentIssue false

Effect of an adequate-protein diet after a low-protein diet on protein catabolism in growing rats

Published online by Cambridge University Press:  24 July 2007

Yoshimitsu Horie
Affiliation:
Laboratory of Nutritional Biochemistry, Department of Agricultural Chemistry, Nagoya University, Chikusa, Nagoya, Japan
Kiyoshi Ashida
Affiliation:
Laboratory of Nutritional Biochemistry, Department of Agricultural Chemistry, Nagoya University, Chikusa, Nagoya, Japan
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. Metabolic alterations related to protein catabolism were studied in rats in transitional states induced by changing from a low-protein (LP) (50 g casein/kg) diet to a high-protein (HP) (250 g casein/kg) diet.

2. Twenty-four hours after the diet was changed, the rats showed a more rapid increase in live-weight gain than controls that had been fed on the HP diet throughout. On the 5th day after the diet change, their increase in body-weight had returned almost to the control rate. Food and therefore nitrogen intakes on the 1st and 5th days after the change in diet were the same as those of the controls. It seems likely therefore that the initial high rate of live-weight gain is an indication of a metabolic adaptation which occurred on the LP diet and which did not fully return to normal until the 5th day after the change of diet.

3. N balance was higher 24 h after the change in diet than in the controls, owing to a reduction in total urinary N and in urea excretion, but when measured on the 5th day it was similar in both groups.

4. Carcass N determination showed that, after 7 d on the LP diet total-, trichloroacetic acid (TCA)-soluble- and TCA-insoluble-N contents (in terms of mg/g rat) were all slightly lower than control values but they had almost returned to normal 5 d after the diet change. There was a significant increase in the TCA-soluble-N content after 24 h on the HP diet to a value greater than the control value.

5. Proteolysis was measured in vitro by incubation of liver slices and diaphragms under anaerobic conditions. With liver slices it was significantly lower 24 h after the diet change than in control rats. On the 5th day it was significantly higher than 24 h after the diet change but had not quite reached the control level. In the diaphragm, proteolysis was also lower 1 d after the diet change, and had not increased at all by the 5th day.

6. Ureogenesis in the liver was reduced significantly 24 h after the diet change and it had almost returned to the control level on the 5th day. On the other hand, arginase (L-arginine amidinohydrolase; EC 3·5·3·1) activity was significantly lower 24 h after the diet change and did return completely to the control level on the 5th day.

7. These results show that the initial increased N balance and reduced N excretion were due to enzymic adaptation to the LP diet, the reduced N excretion being attributable to reduction in hepatic urea production.

Type
Research Article
Copyright
Copyright © The Nutrition Society 1973

References

REFERENCES

Allison, J. B. & Bird, W. C. (1964). In Mammalian Protein Metabolism Vol. 1, p. 483 [Munro, H.N. and Allison, J.B., editors]. New York and London: Academic Press Inc.CrossRefGoogle Scholar
Anson, M. L. & Mirsky, A. E. (1932–3). J. gen. Physiol. 16, 59.CrossRefGoogle Scholar
Archihald, R. M. (1945). J. biol. Chem. 157, 507.CrossRefGoogle Scholar
Ashida, K. & Harper, A. E. (1961). Proc. Soc. exp. Biol. Med. 107, 151.CrossRefGoogle Scholar
Britton, H. T. S. & Robinson, R. A. (1931). J. chem. Soc. p. 1456.CrossRefGoogle Scholar
Brostrom, C. O. & Jeffay, H. (1970). J. biol. Chem. 245, 4001.CrossRefGoogle Scholar
Das, T. K. (1971). Proc. Nutr. Soc. 30, 79A.Google Scholar
Horie, Y. & Ashida, K. (1971). J. Nutr, 101, 1319.CrossRefGoogle Scholar
Korner, A. & Trawer, H. (1957–8). J. gen. Physiol. 41, 219.CrossRefGoogle Scholar
Mendes, C. B. & Waterlow, J. C. (1958). Br. J. Nutr. 12, 74.CrossRefGoogle Scholar
Metz, R., Salter, J. M. & Brunet, G. (1968). Metabolism 17, 158.CrossRefGoogle ScholarPubMed
Muramatsu, K., Sato, T. & Ashida, K. (1963). J. Nutr. 81, 427.CrossRefGoogle Scholar
Schimke, R. T. (1962). J. biol. Chem. 237, 459.CrossRefGoogle Scholar
Schimke, R. T. (1963). J. biol. Chem. 238, 1012.CrossRefGoogle Scholar
Schimke, R. T., Sweeney, E. W. & Berlin, C. M. (1965). J. biol. Chem. 240, 4609.CrossRefGoogle Scholar
Simpson, M. V. (1953). J. biol. Chem. 201, 143.CrossRefGoogle Scholar
Stein, W. H. & Moore, S. (1954). J. Biol. Chem. 211, 915.CrossRefGoogle Scholar
Steinberg, D. & Vaughan, M. (1956). Archs Biochem. Biophys. 65, 93.CrossRefGoogle Scholar
Stephen, J. M. L. & Waterlow, J. C. (1966). Nature, Lond. 211, 978.CrossRefGoogle Scholar
Umaña, R. (1967). Archs Biochem. Biophys. 119, 526.CrossRefGoogle Scholar
Waterlow, J. C. & Stephen, J. M. L. (1966). Br. J. Nutr. 20, 461.CrossRefGoogle Scholar