The metabolic origin of trigonelline in the rat.
A hypothesis of Mason & Kodicek [(1970) Biochem. J. 120, 515-521] that esterified nicotinic acid in niacytin from cereals is a precursor for trigonelline was investigated in rats. Single oral doses of niacytin resulted in the excretion of trigonelline in urine but only in rats that were niacin-deficient and were fed a cereal diet. These animals were found to have an abnormally permeable intestine, which allowed the uptake of molecules not usually absorbed. Orally administered synthetic [14C]nicotinoyl[3H]methylcellulose was shown to be absorbed by niacin-deficient rats on a cereal diet and [14C]trigonelline was excreted in urine. These data indicate that dietary cereal induces a permeability defect in the intestinal mucosa of niacin-deficient rats, which allows the uptake of macromolecular niacytin. The nicotinoyl pyridine nitrogen atom is then methylated and slow hydrolysis releases trigonelline from the macromolecule.
D000470:Alkaloids / Q000378:metabolism* / Q000652:urine; D000818:Animals; D004032:Diet; D002523:Edible Grain; D006020:Glycopeptides / Q000378:metabolism*; D007408:Intestinal Absorption; D008297:Male; D009539:Nicotinic Acids / Q000172:deficiency* / Q000378:metabolism* / Q000652:urine; D010539:Permeability; D051381:Rats
D000470:Alkaloids; D006020:Glycopeptides; D009539:Nicotinic Acids; C008609:niacytin; C034400:nicotinoyl methylcellulose; C009560:trigonelline