INTESTINAL SYNTHESIS 



antiseptics. Ellinger et al. suggested that the pellagra-preventive 

 action of milk, which contains only a small amount of nicotinic acid, 

 may be due to its favourable effect on the intestinal flora, but the 

 pellagragenic action of milk is now attributed to its tryptophan content 

 (page 242). In a further paper, Ellinger et al.^ reported that succinyl 

 sulphathiazole, administered to five subjects, resulted in a 60 % 

 decrease in the urinary output of N^-methylnicotinamide, whereas 

 little reduction in output resulted in three other subjects who were 

 given sulphathiazole, which, being more readily absorbed from the 

 gut than its succinyl derivative, does not appreciably affect the bac- 

 terial population of the intestine. Succinyl sulphathiazole did not 

 bring about inhibition of nicotinamide methylation in vivo, which 

 might have been responsible for the fall in N^-methylnicotinamide 

 output. Ellinger et al. suggested that pellagra may be due to decreased 

 absorption of nicotinamide from the intestinal tract. Subsequently, 

 however, R. Benesch ^ showed that bacteria isolated from faeces at 

 caecostomy were able to synthesise considerable amounts of nicotinic 

 acid under aerobic conditions but that under anaerobic conditions 

 these bacteria actually destroyed nicotinic acid. He suggested that 

 in the normal caecum an equilibrium exists between the two groups 

 of organisms and that disturbance of this equilibrium may lead to 

 nicotinic acid deficiency. 



P. Ellinger and A. Emmanuelowa * used another antibacterial agent 

 to study the phenomenon of intestinal synthesis. This was _^-amino- 

 methylbenzene sulphonamide (marfanil, ambamide), which inhibits 

 the growth of anaerobes, but not of aerobes. They hoped in this way 

 to prevent the growth of organisms that destroyed nicotinic acid 

 without affecting the growth of those that synthesised it. They did 

 in fact find that the output of N^-methylnicotinamide increased, whilst 

 the proportion of anaerobes and coliform organisms decreased and 

 increased respectively. In rats given ambamide, the nicotinamide 

 excretion decreased and then increased. 



The conclusions reached by Ellinger and his colleagues that intes- 

 tinal synthesis may provide part of the nicotinic acid requirements of 

 man received support from the observations of Briggs et al.^ on two 

 subjects who showed symptoms of mild nicotinic acid deficiency. 

 Although maintained on a diet low in trigonelline and providing only 

 3 mg. of nicotinic acid daily, no symptoms of pellagra developed. In 

 one case, nicotinic acid excretion continued low, whilst in the other it 

 was normal ; the trigonelline output was low in both cases and tests 

 for urinary N^-methylnicotinamide were negative. 



According to Denko et al. ^ the faecal excretion of nicotinic acid on a 

 normal diet was higher than the urinary excretion, whilst the combined 

 faecal and urinary output was less than the dietary intake. In this 



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