Choline, unlike most vitamins, can be synthesized by most species, although in many cases, not in sufficient amounts or rapidly enough to satisfy all the animal's needs. For example, when intake of precursors or accessory factors, such as methionine, vitamin B12, or folic acid is insufficient, dogs and cats have been shown to require dietary choline. Young animals also show a higher need for choline than adults. Dog and cat requirements for choline have been determined through the use of purified diets, and recommendations often do not take into account bioavailability from feedstuffs, individual animal variation or effects of other dietary factors.
Dietary factors such as methionine, betaine, myo-inositol, folic acid and vitamin B12 or the combination of different levels and composition of fat, carbohydrate and protein in the diet, as well as the age, sex, caloric intake and growth rate of animals, all have influence on the lipotropic action of choline and thus the requirement of this nutrient (Mookerjea, 1971; DuCoa L.P., 1994). Dietary betaine can spare choline, since choline functions as a methyl donor by forming betaine. In relation to protein level, a larger choline effect on litter size and piglet and litter weight was observed for gilts fed a 12% protein diet than for those fed a 16% protein diet (Maxwell et al., 1987).
Studies have shown that vitamin B12 and folic acid reduce the requirement for choline in chicks and rats (Welch and Couch, 1955). Folic acid and vitamin B12 are required for the synthesis of methyl groups and metabolism of the one-carbon unit. Biosynthesis of a labile methyl group from a formate carbon requires folic acid, while vitamin B12 plays a role in regulated transfer of the methyl group to tetrahydrofolic acid (THF). Therefore, marked increases in choline requirements have been observed under conditions of folic acid and/or vitamin B12 deficiencies.
The two principal methyl donors functioning in animal metabolism are choline and methionine, which contain "biologically labile methyl groups" that can be transferred within the body. This phenomenon is called transmethylation. Therefore, dietary adequacy of both methionine and choline directly affects requirements of each other. Other than exogenous sources of methyl groups from choline and methionine, methyl group formation from de novo synthesis of formate carbons is reduced with folic acid and/or vitamin B12 deficiencies.
Most animals, including dogs and cats, can synthesize sufficient choline for their needs, provided enough methyl groups are supplied. As an example, methionine in the pig can completely replace that portion of the choline needed for transmethylation. Young poultry, on the other hand, are unable to benefit from methionine or betaine as a dietary replacement for choline unless methylaminoethanol or dimethylaminoethanol is in the diet, as young poultry appear unable to methylate aminoethanol when fed a purified diet (Jukes, 1947). Later studies showed that the chick can synthesize microsomal methylaminoethanol and choline from S-adenosylmethionine but, unlike the pig, at an insufficient rate in relation to needs (Norvell and Neshein, 1969).
The metabolic need for choline can be supplied in two ways: either by dietary choline or by choline synthesis in the body, which makes use of labile methyl groups. For selected species, body synthesis sometimes cannot take place fast enough to meet choline needs for rapid growth, and thus clinical signs of deficiency result. Since choline functions in prevention of fatty livers and hemorrhagic kidneys, it does not act as a true vitamin, since choline is incorporated into phospholipids (via cytidine diphosphocholine). Therefore, unlike a typical B-vitamin, the choline molecule becomes an integral part of the structural component of liver, kidney or cartilage cells (Scott et al., 1982).
In general for some species, males are more sensitive to choline deficiency than females (Wilson, 1978). Growth hormone seemed to increase the choline requirement in rats independent of its ability to promote growth and increase food intake (Hall and Bieri, 1953). Cortisone and hydrocortisone have been reported to decrease severity of renal necrosis, and hydrocortisone reduced the amount of liver lipid in choline-deficient rats (Olson, 1959).
Excess dietary protein may increase the young animal's choline requirement. Diets high in fat aggravate choline deficiency and thus increase the growing animal's requirement. Fatty liver is generally enhanced by fats containing a high proportion of long-chain saturated fatty acids. Choline deficiency develops to a greater degree in rapidly growing animals, with deficiency lesions more severe in these animals.
For dogs and cats, choline is only required in the diet when its synthesis from methionine is limiting. This is especially true when high-fat diets are fed, and extensive lipid transport is required (Ralston Purina, 1987).
