The most common signs of choline deficiency in a number of species include poor growth, fatty livers, perosis, hemorrhagic tissue (particularly in kidneys and certain joints), and hypertension. In general, severity of clinical signs in animal species is influenced by other dietary factors, including methionine, vitamin B12, folic acid and dietary fat. When feed intake and consequently growth are depressed by choline deficiency, severity of choline deficiency is then reduced.
Research information is very limited on detection methods to determine choline status of animals. Often the best indicator of status or need for choline is observation of pathology attributable to choline deficiency (e.g., fatty livers) for particular species, as well as beneficial performance responses when diets are supplemented with the vitamin. Tissue levels of choline or its functional metabolites can be determined to evaluate choline status. There is evidence of a reduction of acetylcholine in brains, kidneys and intestines of rats deprived of choline six days after weaning. Choline administered to rats either by injection or by diet causes a dose-related increase in brain acetylcholine (Kuksis and Mookerjea, 1984). Studies on the mechanism of liver fat accumulation have suggested that this is related to a lack of lecithin synthesis. With a choline deficiency, the hepatic phosphatidylcholine:phosphatidylethanolamine ratio is reduced, and is thus a means of evaluating choline status.
For dogs, liver function test as measured by delayed bromsulfalein elimination could be the basis of determining choline status (McKibbin et al., 1944; 1945). Plasma phosphatase activity and blood prothrombin times (impaired vitamin K function) were also elevated in the choline-deficient puppies (NRC, 1985). For cats, hypoalbuminemia (abnormally low level of albumin in the blood plasma) was reported by Mansur Guerios and Hoxter (1962), but was not found by Schaeffer et al. (1982).
