Abstract

A study was made to devise dietary conditions for the induction of simple vitamin B12 deficiency in experimental animals without the delay and complications involved in methods routinely used. Chicks maintained with a purified vitamin B12-deficient diet showed a marked decrease in liver methylmalonyl-CoA mutase activity. Because of the role of vitamin B12 co-enzyme in the metabolism of propionate, branched-chain fatty acids, lysine and isoleucine, a study was carried out to examine the growth of chicks with diets containing these metabolites. The compounds tested included formate, lysine, propionate, butyrate and isoleucine. Vitamin B12 deficiency in terms of growth depression was markedly accentuated by the presence of sodium formate and sodium propionate at 5% levels. None of the other additions had a similar effect when incorporated in the vitamin B12-deficient rations. In rats, vitamin B12 prevented growth depression caused by 2% sodium propionate. In addition, propionate markedly reduced liver methylmalonyl-CoA mutase activity both in the presence and absence of the vitamin in the diet.

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