Hostname: page-component-745bb68f8f-d8cs5 Total loading time: 0 Render date: 2025-01-11T03:11:24.629Z Has data issue: false hasContentIssue false
  • English
  • Français

The effect of dietary restriction on some liver constituents of sheep during late pregnancy and early lactation

Published online by Cambridge University Press:  27 March 2009

E. J. H. Ford
E. J. H. Ford
Affiliation:
A.R.C. Institute of Animal Physiology, Babraham, Cambridge.
Get access Rights & Permissions [Opens in a new window]

Extract

There has been much speculation on the underlying mechanism of pregnancy toxaemia in the ewe (e.g. Reber, 1957; Kronfeld, 1958) and it is generally thought that the condition is a consequence of the failure of the ewe's metabolism to adapt to the increasing hexose demands of the foetus. Insufficient hexose is considered to be produced from dietary propionate and from the deamination of amino acids, with the result that liver glycogen is exhausted, citric acid cycle components are depleted and the resulting failure to oxidize activated acetate gives rise to ketone bodies. If this were the whole sequence of events the clinical symptoms should be reversible by the administration of glucose or glucogenic substances, orally or parenterally. Unfortunately clinical experience is that the condition shows a poor response to glucose therapy and the mortality of field cases is extremely high.

Type
Research Article
Information
The Journal of Agricultural Science , Volume 59 , Issue 1 , August 1962 , pp. 67 - 75
Copyright
Copyright © Cambridge University Press 1962

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

REFERENCES

Bakker, N. & White, R. R. (1957). N.Z. J. Sci. Tech. B, 38, 1001.Google Scholar
Carrol, N. V., Longley, R. W. & Roe, J. H. (1956). J. Biol. Chem. 220, 583.CrossRefGoogle Scholar
Ford, E. J. H. (1959). J. Comp. Path. 69, 20.CrossRefGoogle Scholar
Ford, E. J. H. (1961). J. Comp. Path. 71, 60.CrossRefGoogle Scholar
Ford, E. J. H. & Boyd, J. W. (1960). Res. Vet. Sci. 1, 232.CrossRefGoogle Scholar
Fraser, A. H. H., Godden, W., Snook, L. C. & Thompson, W. (1938). J. Physiol. 94, 346.CrossRefGoogle Scholar
Fraser, A. H. H., Godden, W., Snook, L. C. & Thompson, W. (1939). J. Physiol. 97, 120.CrossRefGoogle Scholar
King, E. J. & Armstrong, A. R. (1934). Canad. Med. Ass. J. 31, 376.Google Scholar
Kronfeld, D. S. (1958). Cornell Vet. 48, 394.Google Scholar
Levvy, G. A. & Marsh, C. A. (1959). Advanc. Carbohyd. Chem. 14, 381.Google Scholar
Miller, L. L. (1948). J. Biol. Chem. 172, 113.CrossRefGoogle Scholar
Parry, H. B. & Shelley, H. J. (1958). J. Physiol. 140, 48P.Google Scholar
Reber, E. F. (1957). N. Amer. Vet. 38, 353.Google Scholar
Robinson, K. W. & Morris, L. R. (1960). Aust. J. Agric. Res. 11, 236.CrossRefGoogle Scholar
Sorenson, N. S. (1957). Nature, Lond., 180, 857.CrossRefGoogle Scholar
Sutherland, E. W. & Cori, C. F. (1951). J. Biol. Chem. 188, 531.CrossRefGoogle Scholar
Weber, G. & Cantero, A. (1957). Science, 126, 977.CrossRefGoogle Scholar