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

Abstract

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.