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Baby pigs fed a vitamin B12-deficient diet for three weeks were co-fed 3 Gm. of “x-methyl” folic acid per kilogram of dry matter of the diet for the next two weeks, which resulted in a marked decrease in growth rate and in the death of five out of twelve pigs.
At the end of the three-week depletion period, the bone marrow showed a rise in nucleated red cells. Following the two-week feeding of the folic acid antagonist the bone marrow became depleted, especially in erythroid elements, and numerous basophilic normoblasts and erythroblasts appeared.
The blood and bone marrow symptoms of this combined vitamin B12-folic acid deficiency were cured by either crystalline vitamin B12 or by folic acid therapy.
Vitamin B12 therapy resulted in optimum growth, while folic acid treatment gave only temporary and suboptimal growth stimulation.
In a second experiment baby pigs were fed a lower protein (20 per cent as compared with 30 per cent in the previous experiment) vitamin B12-folic acid low diet plus Sulfathalidine in an attempt to produce the double deficiency without the use of a folic acid antagonist.
In this experiment a marked reticulocyte response occurred on vitamin B12 therapy followed by a second marked response to folic acid administration.
The vitamin B12-deficient pigs were found to have enlarged thyroids, kidneys, livers, and tongues.
From these two experiments it appears that the pig requires both vitamin B12 and folic acid and that both are involved in hematopoiesis. In addition, vitamin B12 is required for normal growth.
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Received: June 9, 1950
© 1950 Published by Elsevier Inc.