Regulation of tryptophan-niacin metabolism in diabetic rats.

The regulation of tryptophan-niacin metabolism was studied in vivo with regard to the activity of liver ƒ¿-amino-ƒÀcarboxymuconate-c-semialdehyde decarboxylase (picolinic carboxylase) using non-diabetic and diabetic rats. Non-diabetic rats and rats with diabetes induced by alloxan were fed on a commercial diet for 80 days, followed by a niacin-free experimental diet for the next 16 days. Protamine zinc insulin (5units/head) was injected into 3 diabetic rats every 12hr from the 10th to 16th day of the start of administration of the experimental diet. At the 14th day of the experimental diet, 24-hr urine was collected and urine collection repeated after the oral administration of L-tryptophan (100mg/rat). At the end of the metabolic experiments, the content of total nicotinate in liver was determined and the enzyme activity of liver picolinic carboxylase was assayed. The urine was analyzed for N-methylnicotinamide (MNA). The amount of urinary excreted MNA per diet or per administered tryptophan was significantly reduced in diabetes, and insulin treatment rather lessened the amount in spite of normal blood glucose levels. Although the activities of liver picolinic carboxylase in diabetic and insulin-treated diabetic rat groups were higher than that of non-diabetic