The metabolic origin of trigonelline in the rat

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Abstract
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.