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The vitamin nicotinamide is synthesized in the liver from tryptophan, and distributed to non-hepatic tissues. Although it is generally accepted that 60 mg tryptophan is equivalent to 1 mg nicotinamide in humans, the conversion ratio of tryptophan to nicotinamide is changeable. To determine if de novo nicotinamide synthesis from tryptophan is influenced by nicotinamide intake itself, six young women consumed controlled diets containing 30.4 or 24.8 mg niacin-equivalent nicotinamide supplements with 0, 89, 310, or 562 micromol/day (0, 10.9, 37.8, or 68.6 mg/day, respectively), and urinary excretion of intermediates and metabolites of the tryptophan-nicotinamide pathway were measured. Urinary excretion of nicotinamide metabolites increased linearly in a dose-dependent manner. None of the intermediates, including anthranilic acid, kynurenic acid, xanthurenic acid, 3-hydroxyanthranilic acid, and quinolinic acid, changed at all, even when up to 562 micromol/day nicotinamide was given. That is, exogenous nicotinamide did not affect de novo nicotinamide synthesis. Therefore, when niacin equivalent is calculated, the intake of nicotinamide itself need not be considered as a factor that changes the tryptophan-nicotinamide conversion ratio.

To investigate how dietary fiber in the diet affects vitamin B-6 nutriture of rats which have been deprived of vitamin B-6, rats were made vitamin B-6-deficient by feeding a vitamin B-6-deficient 70% casein diet. They were fed 2% cellulose powder-based vitamin B-6-deficient diets supplemented with 3% of additional dietary fiber sources (agar, konjac mannan, pectin and cellulose powder) for subsequent 18 days. Vitamin B-6 status was evaluated according to several biological criteria (weight gain, urinary excretion of xanthurenic acid after tryptophan loading, plasma pyridoxal 5'-phosphate, apparent pyridoxal 5'-phosphate-saturation of liver kynureninase, urinary excretion of 4-pyridoxic acid and fecal output of vitamin B-6). Vitamin B-6 status evaluated by these criteria was considerably improved in the konjac mannan-fed group, when compared with the respective data of the vitamin B-6 supplemented group. The relative mean effect of the konjac mannan diet was about 40% of the vitamin B-6 supplemented diet. In conclusion, konjac mannan was effective for improving the vitamin B-6 nutritional state in vitamin B-6-deprived rats.

Tissue zinc (Zn), copper (Cu) and iron (Fe) were determined in three groups of young male Wistar rats that received a daily pyridoxine hydrochloride (PN.HCl) intake of 45, 23 and 0 micrograms respectively in their diets over 8 weeks. No significant differences were found in the Zn and Cu levels in the liver, kidney, skeletal and cardiac tissue of all 3 groups. The Fe levels were significantly higher in the heart and liver and significantly lower in the skeletal muscle of the group receiving no PN.HCl in the diet (P < 0.05). This study indicates that the increased fecal excretion of Zn and Cu observed during a previous balance study on the above vitamin B6 deficient group of animals may be due to a decreased absorption of these elements from the diet rather than their excretion from tissue stores. The changes in Fe levels in the heart, liver and skeletal muscle points towards some alteration in tissue stores of this element during a vitamin B6 deficiency.

In order to compare the nutritional effect of vitamin B6 derivatives, long-term feeding experiments with rats were carried out using pyridoxine-alpha-D-glucoside (PN-alpha-Glc), pyridoxine-beta-D-glucoside (PN-beta-Glc) or epsilon- (N-phosphopyridoxyl)lysine (PNP-Lys) with test diets consisting of basically the AIN-76 composition, except for the addition of 0.1 mg pyridoxine equivalent (PN eq.)/100 g diet. During 21 days of pair-feeding against the vitamin B6-deficient diet group, body weight gain, urinary excretion of xanthurenic acid and pyridoxic acid were measured. After the feeding experiment, rats were killed and examined in terms of liver kynureninase activity (EC 3.7.1.3) with and without adding exogenous pyridoxal 5'-phosphate (PLP), erythrocyte aspartate aminotransferase activity (EC 2.6.1.1), as well as PLP concentration in blood. Rats fed with PN-alpha-Glc grew well, relative to the PN group. On the contrary, PN-beta-Glc poorly served as vitamin B6 source, because average bioavailability was only about 22% in comparison to that of PN (100%). From this long-term feeding experiments, we have shown that PN-alpha-Glc (average bioavailability about 84%) is a good source of vitamin B6 similar to PN.

In a bipartite rearing experiment (day 1-24 and 24-45) 72 early-weaned piglets were used to study the effect of varying dietary vitamin B6 contents on renal excretion of xanthurenic and kynurenic acid after a tryptophan load, on urea concentration and activities of two transaminases in serum at the end of each period. The animals, divided into 6 groups, were fed ad libitum a prestarter and a starter in period I and II, respectively, each containing 0.5, 1.2, 2.0, 2.8, 3.5 or 6.6 mg vitamin B6 per kg dry matter. The urinary xanthurenic acid excretion was elevated especially at the vitamin B6 supply of 0.5 ppm and rose severalfold with increasing depletion time (period II). In both periods, the smallest amount was excreted by piglets supplemented with 2.8 ppm. In comparison to groups B (1.2 ppm) and C (2.0 ppm), their average excretion rate was reduced by 29% and 15%, respectively, in period I and by 50% and 22%, respectively, in period II. Analogously to xanthurenic acid, the smallest amount of kynurenic acid was excreted by group D (2.8 ppm). Starting from the lowest vitamin B6 supply, the activity of SGPT showed an almost linear increase in both experimental periods. In contrast, SGOT already reached an upper activity level with the dietary vitamin B6 content of 3.5 and 2.8 ppm at the end of period I and II, respectively. The concentration of serum urea was influenced only by the lowest vitamin B6 supply of 0.5 ppm.