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Journal of Nutrition Vol. 99 No. 3 November 1969, pp. 288-292
Copyright © 1969 by American Society for Nutrition
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The Role of Dietary Fat in Protecting the Rat against Oxythiamine-produced Thiamine Deficiency1,2,

Carl D. Bennett3, James H. Jones and June Nelson

Laboratories of Biochemistry, Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania

Dietary fat decreases the thiamine requirements of the rat and provides extended protection against the thiamine antagonist oxythiamine. We have measured the changes in the activities of three major thiamine-requiring enzymes of the brain and liver in rats fed low fat and high fat oxythiamine diets. Brain activities were unchanged with both diets. Liver and blood transketolase activities were decreased to the same extent with both diets. With the high fat oxythiamine diet, the oxidation of pyruvate by the liver was decreased to 51% of the control, whereas with the low-fat oxythiamine diet, it was decreased to 26% of the control (significantly lower than for the high-fat oxythiamine diet). These data provide additional evidence to support the idea that dietary fat spares thiamine by supplying energy through a route which requires a minimum of thiamine. On the basis of the results from our study, it appears that the cause of death in the thiamine deficiency produced by oxythiamine is a decreased ability of the rat to convert dietary carbohydrate into utilizable energy. The importance of the hexose monophosphate shunt in the metabolism of fat is discussed.


1 A preliminary note presenting some of the data given here has been published (Nature, 220: 1236, 1968).

2 Supported in part by Public Health Service Grant no. NB-03626 from the National Institute of Neurological Diseases and Blindness.

3 Fellow of the Institute of Neurological Sciences, University of Pennsylvania, United States Public Health Service Trainee-5T1-GM 281, and National Institute of Neurological Diseases and Blindness Post-doctoral Fellow F2-NB-32,947. Present address: Dept. of Biochemistry, School of Medicine, Yale University, New Haven, Connecticut 06510.

Manuscript received 16 June 1969.





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