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Male rats about 100 days old were fed a B-6 deficient diet supplemented with 4'-deoxypyridoxine (1 g/kg diet) and/or pyridoxine hydrochloride (22 mg/kg diet) for 30 to 35 days. Addition of 4'-deoxypyridoxine to the B-6-deficient diet produced greater losses in body weight (P less than 0.05) and thymus weight (P less than 0.01) than in B-6-deficient pair-fed controls. 4'-Deoxypyridoxine combined with a B-6-deficient diet produced no decreases in the concentration of pyridoxal phosphate or pyridoxine kinase in the tissues examined when compared with B-6-deficient controls. Addition of deoxypyridoxine to a diet containing adequate B-6 tended to reduce that absolute weight of the adrenal glands and increased (P less than 0.05) plasma cholesterol compared with animals receiving only vitamin B-6. Compared with the B-6-deficient groups, pyridoxal phosphate concentrations in animals receiving normal B-6 were significantly (P less than 0.01) increased in the liver, muscle and adrenal glands but not in the thymus. In all groups the pyridoxine kinase activity was highest in the adrenal glands (3.6-6.3 pmole pyridoxine phosphate/minute/mg tissue) followed by the liver (1.3-3.7) and thymus (0.7-1.3). These high kinase values and the weight changes suggest an important role for vitamin B-6 in these organs. Recent evidence that pyridoxal phosphate may interact with glucocorticoid receptors raises the possibility that the role of vitamin B-6 in these and other organs may involve metabolic regulation by a mechanism independent of the well-established coenzyme function of this vitamin.

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Feeding of lactose in amounts comparable to the adult human intake in developed countries (6% of diet, and in later studies 10%) had no major effect on cholesterol and bile acid metabolism of germ-free and conventional rats. However, when lactose-containing casein-starch diets were sterilized by autoclaving, changes in intestinal and/or fecal bile acids were found. Both germ-free and conventional rats demonstrated some increase in intestinal beta-muricholic acid concentrations ascribable to the mere presence of lactose in the diet. Autoclaving of the diet produced additional changes, especially in the fecal bile acid pattern of conventional rats. Here the ratio between the beta-muricholic-derived secondary bile acids hyodeoxycholic and omega-muricholic acids changed from the usual 5:3 to approximately 1:10, with omega-muricholic acid becoming the major fecal bile acid. These changes point to a notable effect of lactose-derived products, formed during steam-sterilization, on the microbial modification of intestinal bile acids in the lower gut. Similar changes have been observed after oral administration of aureomycin and other, unrelated antibiotics that inhibit growth of gram positive organisms.