The role of the pancreas in vitamin B 12 absorption: studies of vitamin B 12 absorption in partially pancreatectomized rats.
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The effect of partial pancreatectomy (80-90%) on vitamin B(12) absorption was studied in the rat. The absorption of 5 ng of (57)Co-labeled vitamin B(12) was significantly reduced from 70 +/-2.5% (mean +/-SE) in control and sham-operated rats to 32 +/-2.6% in partially pancreatectomized rats. Hog pancreatic extract (0.17 g/kg) improved vitamin B(12) absorption from 30.0 to 61.0% in partially pancreatectomized rats but did not alter vitamin B(12) absorption in control rats. Chloramphenicol did not enhance vitamin B(12) absorption in partially pancreatectomized rats with pancreatic extract-improved vitamin B(12) malabsorption. The partially pancreatectomized rats with pancreatic extract-improved vitamin B(12) malabsorption were sacrificed and the stomach and small bowel studied in vitro to further define the pathogenesis of the vitamin B(12) malabsorption. Rat gastric intrinsic factor stimulated vitamin B(12) uptake by intestinal sacs prepared from partially pancreatectomized rats 3.1-fold. Gastric intrinsic factor prepared from partially pancreatectomized rats was as effective in promoting vitamin B(12) uptake by rat intestinal sacs as intrinsic factor prepared from control rats. These data indicate that partially pancreatectomized rats develop an abnormality in the absorption of labeled vitamin B(12) which can be corrected by pancreatic extract. The vitamin B(12) malabsorption is due to neither an alteration in gastric intrinsic factor activity nor an impairment of the intrinsic factor-vitamin B(12) receptor in the intestine. It is suggested that in the partially pancreatectomized rats the intrinsic factor-vitamin B(12) complex exists in a form which is not available for absorption. (+info)
A simple assay of intrinsic factor-vitamin B12 complex employing the binding intrinsic factor antibody.
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The reaction between binding intrinsic factor antibody and intrinsic factor-vitamin B(12) complex has been studied. Initially in the zone of antibody excess, the relationship between the amount of antigen present and the amount of antigen-antibody complex adsorbed onto zirconium phosphate gel was linear. With increasing amounts of antigen, the curve departed from linearity and reached a plateau. The linear portion of the reaction forms the basis of a simple and reproducible assay for quantitating intrinsic factor to which vitamin B(12) has already been bound. The assay provides a method for studying the fate of intrinsic factor-vitamin B(12) complex during digestion and absorption. In two normal subjects given radioactive vitamin B(12) orally, aspiration of ileal contents showed that only 50 to 70% of the radioactivity was bound to intrinsic factor at that level. (+info)
Immunogenicity of rabies virus inactivated by -propiolactone, acetylethyleneimine, and ionizing irradiation.
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Ionizing radiation, beta-propiolactone, and acetylethyleneimine were compared for their ability as virus-inactivating agents for the preparation of rabies vaccine. Each agent reduced viral infectivity exponentially; ionizing radiation also destroyed viral hemagglutinin. The vaccine prepared by ionizing radiation was equal or superior to that prepared by beta-propiolactone in its ability to protect mice from rabies infection. The acetylethyleneimine-treated vaccine was a less potent immunogen. (+info)
Role of third serum vitamin B 12 binding protein in vitamin B 12 transport.
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A third vitamin B(12) binding protein present in normal serum has been shown to participate in transport of labelled vitamin B(12) absorbed from the gut. All three vitamin B(12) binding proteins in serum were labelled at the same time after oral administration of vitamin B(12), implying that "free" vitamin B(12) reached the portal blood from the gut mucosa. (+info)
Transport function of transcobalamin II.
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The uptake of free and bound (57)CoB(12), principally to transcobalamin II (TC II), was studied in isolated, perfused liver and kidney of the dog. (1) There was good uptake of canine TC II-B(12) by both organs. (2) In the liver TC II enhanced uptake over that of free B-12. (3) Renal uptake of free B-12 was greater than that of TC II-B(12). Free B-12 was neither lost in the urine nor returned to the circulation. (4) On a per gram tissue basis, renal uptake of TC II-B(12) was greater than hepatic. (5) There was renal release or production of TC II (6) Some TC II but more of a larger molecular size binder came from the liver. (7) Passing free B-12 through the kidney enhanced its uptake by the liver. (8) Passing free B-12 through the liver depressed its uptake by the kidney. (9) It is postulated that the distribution of B-12 can be modified by (a) different responses of tissue to TC II-B(12), (b) synthesis of TC II by an organ, and (c) the effects of B-12 passing through one organ to another. (+info)
Competitive nature of the intestinal transport mechanism for cobalt and iron in the rat.
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Dose- and time-response studies were performed in iron-loaded and iron-deficient rats in order to define, (a) the kinetics of absorption of cobalt and iron, (b) the nature of the inhibitory effect of one metal on the absorption of the other, and (c) the effect of variations in body iron stores on these processes. The duodenum was perfused for 5-90 min with labeled solutions containing 5.0 mM iron or 5.0 mM cobalt. In iron-loaded rats, the rate of cobalt absorption was constant for 90 min whereas the rate of iron absorption fell after 30 min. In comparison to these results, the rate of absorption of both metals was increased in iron deficiency, and was more rapid in the first 30 min than in the 30-90 min period.To determine the response to varying doses of metal, we perfused duodenal loops for 30 min with 0.1-10.0 mM solutions of either iron or cobalt. In both iron-loaded and iron-deficient groups, a greater proportion of the metals was absorbed from smaller than from larger doses. When iron and cobalt were perfused together in iron-deficient animals, cobalt competitively inhibited iron absorption, and conversely, iron reduced cobalt absorption. The apparent maximum transport velocity was similar for both metals, but the affinity for cobalt was greater than iron. The results suggest that the absorption of cobalt and iron is mediated by a transport system in which two processes operate simultaneously; the first is limited largely by the concentration of available metal in the lumen of the intestine, whereas the second process depends upon the activity of a mechanism which displays saturation kinetics and competitive inhibition. The former process prevails when iron stores are replete, whereas the latter predominates when there is a need for iron, such as in iron deficiency. (+info)
Effect of pH changes on the binding of vitamin B12 by intrinsic factor.
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The binding of vitamin B(12) by human gastric juice has been found to be pH dependent. Maximum binding occurs between pH 6.5 and 10. Outside this pH range the vitamin B(12)-binding ability of human gastric juice decreases and at pH below 2 or above 12.2 this drops sharply to about 10 to 15% of the maximum. Three commercial hog intrinsic factors have been found to give a similar response to pH changes. The pH-dependent binder in human gastric juice has been shown to be intrinsic factor by the addition of intrinsic factor-blocking antibody. About 10% of vitamin B(12) bound by human gastric juice is not bound by intrinsic factor and is not pH dependent. The reduction in the vitamin B(12)-binding capacity of human gastric juice induced by an adverse pH is reversed by neutralization. The physiological and clinical significance of these observations is discussed and their relevance to various procedures in vitro noted. (+info)
Disseminated amyloidosis in germfree mice. Spontaneous prevalence, relationship to ionizing radiation and pathogenetic implications.
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Spontaneous amyloidosis was noted in a significant number of germfree mice in comparison with their conventional contemporaries. The adjusted prevalence of this disease was increased in both groups by whole-body exposure at 6 weeks of age to 700 rad of ionizing radiation. The germfree groups demonstrated persistent hypogammaglobulinemia throughout their lifespans and no evidence of significant inflammatory processes at necropsy. The possible interpretation of these observations is discussed and it is concluded that defective or deficient immunoglobulin production may be the essential prerequisite for the development of amyloidosis. (+info)