Effect of tryptophan intake on oxidation of [7a-14C]tryptophan and urinary excretion on N1-methylnicotinamide in the rat.

Oxidation of tryptophan and urinary excretion of niacin metabolites were studied in weanling rats fed ad libitum for 12 to 16 days niacin-free and nicotinamide-supplemented (20 mg/kg of diet) diets containing 15% of crystalline amino acids and from 0.04 to 1.0% of L-tryptophan. N1-methylnicotinamide was measured in urine collected during the last 3 days of the feeding period. After the feeding period, rats were placed in metabolic cages, and each rat was given 4 g (dry weight) of diet containing a tracer dose of DL-[7a-14C]tryptophan. Expired CO2 was collected hourly for 10 hours. In both the niacin-free and nicotinamide-supplemented groups, weight gains increased with increasing increments of tryptophan up to about 0.16% L-tryptophan. With more than 0.16% of L-tryptophan, the amount of N1-methylnicotinamide excreted per day by both groups of rats increased linearly with increasing tryptophan intake, but proportionately less N1-methylnicotinamide was excreted when the dietary tryptophan level was 1.0%. The amount of tryptophan oxidized per 10 hours increased linearly with increasing dietary tryptophan levels between 0.16 and 1.0%. Therefore, the decline in excretion of N1-methylnicotinamide with the 1.0% tryptophan level could not be accounted for by increased oxidation. These results suggest that after the tryptophan requirement for growth is met, the amount of tryptophan oxidized and converted to nicotinamide is directly proportional to the level of tryptophan intake up to about 3 times the requirement for growth. The tryptophan requirement of the growing rat fed niacin-free and nicotinamide-supplemented diets estimated from the inflection points of N1-methylnicotinamide excretion curves was in good agreement with the requirement of about 100 mumoles/day determined from the growth curve.

NAD glycohydrolase activity in the liver of rats fed on excess leucine diet and low or high protein diet.

In rats fed for 2 weeks on a 10% casein diet supplemented with 5% leucine, the hepatic NAD content was lowered when comparing with the control rats pair-fed on the 10% casein diet. The hepatic NAD glycohydrolase [EC 3.2.2.5] activity increased by 25% in the leucine-supplemented diet-fed rats and by 40% in the nicotinic acid-free diet-fed rats. The hepatic NAD glycohydrolase activity in the rats fed on the nonprotein diet freely for 1 week was elevated by 60% compared to the rats fed on the 18% casein diet. The hepatic NAD content in the former animals was significantly lower than that in the latter. The 70% casein diet caused changes in neither hepatic NAD content nor NAD glycohydrolase activity. These results indicated an inverse relationship between hepatic NAD content and NAD glycohydrolase activity.

Effect of nicotinic acid on cerebroside synthesis in rat brain.

The effect of nicotinic acid on the synthesis of cerebrosides in the brain was studied during brain development. The concentration of cerebrosides in the brain was significantly lower in nicotinic acid-deficient animals than in those receiving a nicotinic acid-supplemented diet. The total lipid concentration in the brain of nicotinic acid-deficient rats was slightly lower than that of rats fed on the nicotinic acid-supplemented diet. Therefore, the ratio of cerebrosides to total lipids of nicotinic acid-deficient rats was markedly lower than that of nicotinic acid-supplemented rats. However, this low cerebroside level in nicotinic acid-deficient rats was restored by the administration of the nicotinic acid-supplemented diet. Synthesis of cerebrosides was followed in the brain of developing rats after intracerebral injection of L-[U]14C]serine. The total amount of radioactivity incorporated into the cerebroside fraction of nicotinic acid-deficient rat was smaller than that of nicotinic acid supplemented rats. These observations suggest that nicotinic acid affects cerebroside synthesis in the brain of rats.

The effect of a high level of dietary leucine on the niacin status of chicks and rats.

Baby chicks were fed purified diets containing 90 g/kg casein and 100 g/kg gelatin. With low levels of niacin and tryptophan, niacin deficiency resulted: this was not exacerbated by the addition of supplementary leucine (17.4 g/kg). With levels of niacin and tryptophan that supported rapid growth the further addition of supplementary leucine depressed food consumption and weight gain; in most instances this was statistically significant. No evidence was obtained to indicate that a high level of dietary leucine could result in niacin deficiency in chicks. Comparable experiments were carried out with weanling rats given a basal diet containing 60 g/kg casein and 60 g/kg gelatin. Adding 15 g/kg L-leucine gave results similar to those obtained with chicks and the same conclusions were drawn.

The effect of a high level of dietary leucine on the niacin status of dogs.

Two feeding trials were designed to precipitate niacin deficiency in puppies receiving low levels of niacin by adding 15 g/kg supplementary l-leucine to a diet containing 180 g/kg casein. We failed to produce such an effect and, as niacin levels were gradually reduced, the times at which control dogs became deficient (and then responded to injections of the vitamin) were not significantly different from those for dogs receiving the leucine supplement. Differences between the conditions of our experiments and of the experiment in which this effect was found are discussed. Two pairs of littermates in trial 2 died suddenly while apparently in fairly good condition, but revealing fatty livers and/or changes in heart muscle on autopsy. Similar observations have been reported by others using purified diets with dogs over long periods; there is no certain explanation.

Nutritional status of long-stay geriatric in-patients: effects of a food supplement (Complan).

In a detailed nutritional study of 50 long-stay elderly patients, intakes of vitamins C and D and nicotinic acid were found to be sub-optimal compared to D.H.S.S. recommendations. Whole-food supplementation did not increase calorie, fat or carbohydrate intake, although it did increase protein, vitamins and minerals. However, it did not correct the intake of vitamins C and D and of nicotinic acid to those recommended by D.H.S.S. Supplementation affected neither serum albumin nor transferrin. No positive correlation could be established between physical disabilities and total dietary intake among these patients. However, the appearance of the skin improved and skin thickness increased in the supplemented patients and the blood urea diminished in them also.

Effect of nicotinic acid on catecholamine synthesis in rat brain.

Effect of nicotinic acid on the formation of catecholamine has been studied. Norepinephrine and dopamine concentrations in brain were 30 per cent higher and brain catecholamine formation was 50 per cent higher in the nicotinic acid-supplemented rats than the nicotinic acid-deficient rats. However, these catecholamine levels of the nicotinic acid-deficient rats were recovered by the administration of nicotinic acid. The concentration of brain tyrosine was unaltered after administration of nicotinic acid to the nicotinic acid-deficient rats. Therefore, the changes catecholamine formation by the nicotinic acid supplementation were not due to the difference of tyrosine concentration in the brain which is the precursor for catecholamine biosynthesis. As the difference of catecholamine concentration between the nicotinic acid deficient and the nicotinic acid supplemented group was smaller than that of catecholamine formation of these groups, the turnover of catecholamine was supposed to be decreased in nicotinic acid deficiency.