features of vitamin B12 is that it contains 4.5 percent cobalt. The naturally occurring forms of vitamin B12 are adenosyl-cobalamin and methylcobalamin and these are found in plant and animal tissues. Cyanocobalamin, an artificially produced form of vitamin B, is used extensively because it is relatively stable and readily available. The primary functions of vitamin B12 involve metabolism of nucleic acids and proteins, in addition to metabolism of fats and carbohydrates. Specifically, this vitamin plays a role in purine and pyrimidine synthesis, transfer of methyl groups, protein formation, and metabolism of fats and carbohydrates. Vitamin B12 is of special interest in ruminant nutrition because of its role in propionate metabolism (Marston et al., 1961) and the practical incidence of vitamin-B12 deficiency as a secondary result of cobalt deficiency. The ruminant’s requirement for vitamin B12 is higher than the nonruminant’s requirement and is associated with the requirement for cobalt, since this trace mineral is a component of vitamin B12. Cobalt content of the diet is the primary limiting factor for ruminal microorganism synthesis of vitamin B12. Substantial areas of the United States, Australia, and New Zealand have soils without enough cobalt to produce adequate concentrations in plants to support optimum vitamin B12 synthesis in the rumen (Ammerman, 1970). (For additional information on cobalt, see Chapter 5.)
A vitamin-B12 deficiency is difficult to distinguish from a cobalt deficiency. The signs of deficiency may not be specific and can include poor appetite, retarded growth, and poor condition. In severe deficiencies, muscular weakness and demyelination of peripheral nerves occurs. In young ruminant animals, vitamin-B12 deficiency can occur when rumen microbial flora are not yet fully developed.
Thiamin functions in all cells as a coenzyme cocarboxylase. Thiamin is the coenzyme responsible for all enzymatic carboxylations of a-keto acids in the tricarboxylic acid cycle, which provides energy to the body. Thiamin also plays a key role in glucose metabolism, as a coenzyme in the pentose phosphate pathway.
Thiamin antimetabolites have been found in raw fish products and bracken fern (Somogyi, 1973). Polioencephalomalacia (PEM), a central nervous system disorder, in grain-fed cattle and sheep has been linked to thiaminase activity or production of a thiamin antimetabolite in the rumen (Loew and Dunlop, 1972; Sapienza and Brent 1974). Affected animals have responded to intravenous administration of thiamin (2.2 mg/kg BW). Thiamin analogs produced in the rumen by thiaminase I in the presence of a cosubstrate appeared to be responsible for PEM (Brent and Bartley, 1984). Supplementation of high-concentrate diets with thiamin, however, yield inconsistent results (Grigat and Mathison, 1982, 1983).
Synthesis of thiamin by rumen microflora makes it difficult to establish a ruminant requirement. Animals with a functional rumen can generally synthesize an adequate amount of thiamin. However, the synthesis of thiamin is subject to dietary factors including levels of carbohydrate and nitrogen. In addition, high sulfur diets have been associated with thiamin deficiency and PEM, a laminar softening or degeneration of brain gray matter in steers (Gould et al., 1991). Animal size, genetic factors, and physiological status also influence thiamin requirements.
In all species, a thiamin deficiency results in central nervous system disorders, since thiamin is an important component of the biochemical reactions that break down glucose to supply energy to the brain. Other signs of thiamin deficiency include weakness, retracted head, and cardiac arrhythmia. As with other water-soluble vitamins, deficiencies can result in slowed growth, anorexia, and diarrhea.
Niacin functions in carbohydrate, protein and lipid metabolism as a component of the coenzyme forms of nicotinamide, nicotinamide adenine dinucleotide (NAD), and nicotinamide adenine dinucleotide phosphate (NADP). Niacin is particularly important in ruminants because it is required for liver detoxification of portal blood NH3 to urea and liver metabolism of ketones in ketosis.
Niacin has been reported to enhance protein synthesis by ruminal microorganisms (Riddell et al., 1980, 1981). Niacin synthesis in the rumen seemed adequate when no niacin was added to the diet; however, when 6 g was added per day, an increase in niacin flow from the rumen occurred (Riddell et al., 1985). Supplemental niacin was more effective in increasing microbial protein synthesis with urea than soybean meal (Brent and Bartley, 1984). Responses to supplemental niacin of feedlot cattle have been variable.
Niacin is supplied to the ruminant from three primary sources: dietary niacin, conversion of tryptophan to niacin, and ruminal synthesis. Although niacin is normally synthesized in adequate quantities in the rumen, there are several factors that can influence ruminant niacin requirements (Olentine, 1984). These factors include protein (amino acid) balance, dietary energy supply, dietary rancidity, de novo synthesis, and availability of niacin in feeds. Excess leucine, arginine, and glycine increase the niacin requirement; whereas increasing dietary tryptophan decreases the