Choline, unlike most vitamins, can be synthesized by most species, although in many cases not in sufficient amounts or rapidly enough to satisfy all of the animal's needs. Dietary sources can meet metabolic requirements for choline, or choline can be synthesized in vivo from labile methyl groups. Methyl groups can originate from methionine (in excess of that required for protein synthesis), and therefore, level of dietary methionine affects the requirement for choline. Kroening and Pond (1967) fed 5 kg (11 lb) pigs a low-protein (12%) diet supplemented with three levels of dl-methionine (0, 0.11% or 0.22%). The addition of 1,646 mg of choline per kg (748 mg per lb) of diet improved the weight gains and feed conversion of pigs fed the control and the 0.11% but not the 0.22% methionine-supplemented diet. Nesheim and Johnson (1950) reported that baby pigs supplied with diets containing 1.6% methionine did not require dietary choline supplementation based on growth and feed efficiency. Likewise, for starting, growing and finishing pigs, the North Central Region-42 Committee on Swine Nutrition (1980) reported that added choline was not beneficial as assessed by performance of pigs fed corn-soy-lysine diets. In their evaluation, performance of starter, grower and finisher pigs fed diets supplemented with up to 246, 396 and 396 mg choline per kg diet, respectively, was compared with that of pigs that did not receive supplemental choline. Russett et al. (1979b) reported that starter pigs do not require more than 520 mg choline per kg of diet when fed an 18% crude protein, corn-isolated diet (0.23% cystine) that provided 0.22% methionine. The basal diet was analyzed to provide 440 mg choline per kg diet. Russett et al. (1979b) found no benefit of choline supplementation on performance. These results are in agreement with those of Stockland and Blaylock (1974), who reported that 412 mg of supplemental choline per kg of ration was adequate to provide optimum sow and gilt performance. Seerley et al. (1981) found no beneficial effect on piglet survival or lipid mobilization when 500 ppm supplemental choline was included in the diets of sows throughout lactation.
The choline requirement for growing pigs ranges from 300 to 600 mg per kg (136 to 272 mg per lb) of diet, while adult swine require 1,000 to 1,250 mg per kg (568 mg per lb) (NRC, 1998). Estimates of choline requirements are based on the assumption that the diets contained an adequate level of methionine. Requirements for choline have generally 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. In addition to methionine or other sulfur amino acids, additional dietary factors, such as betaine, myoinositol, folic acid and vitamin B12; the combination of different levels and composition of fat, carbohydrate and protein in the diet; and the age, sex, caloric intake and growth rate of animals all influence the lipotropic action of choline and thereby requirement of this nutrient (Mookerjea, 1971). 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).
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 methionine and choline directly affect requirements of each other (Russett et al., 1979a). Other than exogenous sources of methyl groups from choline and methionine, methyl group formation from de novo synthesis of formate carbons is reduced with folate and (or) vitamin B12 deficiencies.
Most animals 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 contrary, 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). A later study 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 Nesheim, 1969).
The metabolic need for choline can be supplied in two ways: either by dietary choline or by choline synthesis in 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 acts to prevent fatty livers and hemorrhagic kidneys, it does not act as a true vitamin, as it 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 hepatic lipid choline deficiency in rats (Olson, 1959).
Excessive 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. Boyd et al. (1982) conducted studies to investigate possible choline-tallow interactions when fed to sows. No choline-tallow interaction or response to supplemental choline at 220 and 770 mg was observed for preweaning pig performance. Choline deficiency develops to a greater degree in rapidly growing animals, with deficiency lesions more severe in these animals.
