| Abstract: | Thiamin analogs, produced in the rumen by thiaminase I, in the presence of a cosubstrate appear to be responsible for the central nervous system disorder, polioencephalomalacia (PEM). For PEM to occur, an analog must be produced that inhibits an essential thiamin-requiring reaction, and results from a cosubstrate present in the rumen. In high concentrate diets, thiaminase I is produced by rumen microbes. However, PEM can also be caused by thiaminase I of plant origin. Based on physical characteristics and cosubstrate specificity, the thiaminase I enzymes produced by Bacillus thiaminolyticus and Clostridium sporogenes appear to be different from the enzyme produced by the rumen. Because niacin and certain antihelmentics are thiaminase I cosubstrates, they should be used cautiously. Supplementary niacin increased microbial protein synthesis in vitro and in vivo, and was more effective with urea than soybean meal. Supplementary niacin (5 to 6 g X cow-1 X d-1) increased milk production in postpartum cows but not in those in mid-lactation, and in cows fed soybean meal but not in those fed urea. We believe the heating of soybean meal during commercial processing decreased the availability of niacin for rumen protozoa. Supplementary niacin for postpartum cows increased blood glucose, decreased blood ketones and reduced the incidence of ketosis. Niacin flow to the small intestine and its absorption from the small intestine increased with niacin supplementation. Supplemental niacin prevented the postpartum decrease in red blood cell niacin observed in control cows. |
