A study of starvation ketosis in the ruminant.

There is a theory of long standing that post-parturient dyspepsia of cattle, or bovine ketosis as it is often called, is caused by an inadequate calorie intake; the same has also been suggested of the condition known as pregnancy toxaemia in ewes. It was felt, therefore, that it might be of value to make a detailed study of starvation ketosis in those animals, especially as earlier experiments appear to have yielded rather conflicting results. Thus Sjollema & Van der Zande (1923), who carried out one of the earliest experiments on starvation ketosis, came to the conclusion that the cow does not readily produce much acetone unless in certain diseased conditions. Similarly Carpenter (1927) concluded that the ruminant was quite resistant to starvation ketosis. However, Forbes (1943) claimed to find a rise in blood ketone bodies in lactating cows kept on submaintenance diets for considerable periods, and both Carlstrom (1950) and Holmes (1950) noted a marked urinary excretion of ketone bodies by cows starved postpartum. Similarly, Sampson & Boley (1940) and Clark, Groenewald & Malan (1943) produced a starvation ketosis in ewes in late pregnancy, and the latter workers succeeded, by prolonged feeding of inadequate rations, in producing it also in non-pregnant sheep. Few workers, however, have made any really detailed biochemical study of the ketosis observed, and we decided, therefore, to apply to this problem the methods for determining ketone bodies already elaborated by us (Thin & Robertson, 1952).