ABSTRACT
Our findings in this study show (a) that hepatic uptake can be substantially increased even after injury, by the additon of a strong binding substance, preferably in its purified form, to vitamin B12 upon parenteral administration, (b) hepatic uptake for vitamin B12 can be enhanced further by mixing increasing doses of the intrinsic factor to vitamin B12 upon administration, (c) vitamin B12 mixed with intrinsic factor does not readily diffuse to storage depots, but rather remains at the site of injection, when administered by the intramuscular route, (d) vitamin B12-intrinsic factor complex is held more tenaciously by the liver than vitamin B12 alone. (Summary and conclusion)
ABSTRACT
Our findings indicate: (a) an elevation of vitamin B12 values in the sera of patients with various form of liver disease where the rise in serum level is two to three times the control value; (b) the common denominator in the increase of serum vitamin B12 level is the presence of hepatocellular mechanism responsible for this damage; (c) the most logical elevated values is the release of stored vitamin B12 in the liver. (Summary)
ABSTRACT
The data presented in this study clearly demostrate:(a) liver damage induced by chemical agents increased significantly serum vitamin B12 level and at the same time diminished liver B12 concentration, (b) the increase of B12 level in the serum is attributable mainly to vitamin B12 activity and not to alkali stable factors in the serum, (c) the absorption of orally administered vitamin B12 labelled Co60 is not influenced by existing high vitamin B12 level in the serum liver injury, (d) the increased level of serum vitamin Br after liver injury is largely due to the mobilization of vitamin B12 stores in the liver, (e) hepatic uptake of radioactive vitamin B12Co60 is considerably diminished after the induction of liver damage, (f) parenteral administration of vitamin B12Co60 after injury increased urinary excretion of radioactivity. (Summary and conclusion)