Excretion Of Vitamin B12 Research Articles

Endogenous ethanol-producing bacteria interference in pathogen-host crosstalk.

The host micronutrient milieu is a compilation of factors of both endogenous and exogenous origin. This milieu shapes the host's immune responses and can control the inflammatory response of the host when infected. Among vitamins, B12 plays a key role in the defense process because there is intense competition for it between pathogenic invaders and infected host cells. Alcoholic beverages and antibiotics can cause biological (in vivo) interferences that affectpathogen-host crosstalk. Ethanol is known to interfere with the absorption, distribution, and excretion of vitamin B12 in men and animals. However, the molecular mechanisms underlying this backdrop are not fully understood. Here we explored how Gram-positive ethanol-producing and Gram-negative vitamin B12-producing microbes of the infected milieu interact to influence biomarkers of host cell defense responses in absorbing, digesting, and defensive cells. We investigated two different cell types of colon and liver origin, hepatic-like Huh7 cells and HT- 29/B6 colon cells. To assess the ability of secreted factors from bacteria to exert influence on co-cultured cell's secretion of host-defense markers in response to invading pathogens, co-cultured human colonic HT-29/B6 and human hepatic Huh-7 (hereafter Huh7) cells were stimulated or not with Klebsiella pneumoniae 52145 for 24 h in the presence or absence of either Weissella confusa strain NRRL-B-14171 (as a Gram-positive producer of ethanol), Limosilactobacillus reuteri 20016 (as a Gram-positive producer of vitamin B12), or Pseudomonas nitroreducens 1650 (as a Gram-negative producer of vitamin B12). After stimulation, molecular functional biomarkers of host cell defense responses including total MMP-1, lysozyme activity, ALP, and IL-25 were measured. While simultaneously reducing IL-25 secretion, Kp52145 alone significantly elicited MMP-1, lysozyme, and ALP secretion from co-cultured cells, as compared to no treatment. When compared with Kp 52145 stimulation alone, Pn1650 significantly potentiated MMP-1 and lysozyme secretions from Kp 52145-stimulated co-cultured cells by 29.7% and 67.4%, respectively. Simultaneously, a potentiated suppression (an overall decrease of 77.3%) in IL-25 secretion occurred 24 hours after Kn52145 plus Pn1650 administration. Compared to Kp52145-stimulation alone, treatment with W. confusa NRRL-B-14171 and Kp52145-stimulated co-cultured cells was associated with significant additive induction of MMP-1 and lysozyme secretions. However, compared to Kp52145-stimulation alone, W. confusa NRRL-B-14171 treatment significantly potentiated Kp52145-induced suppression of IL-25. using the same condition as mentioned above and compared to Kp52145-stimulation alone, L. reuteri 20016 treatment altered the secretion pattern in response to Kp52145: L. reuteri 20016-treated cells displayed less aversive responses towards Kp52145, suggesting that L. reuteri 20016 modulation may act differently on Kp52145 - induced signaling.

Urinary excretion of vitamin B12 depends on urine volume in Japanese female university students and elderly

Recent studies have shown that urinary excretion of water-soluble vitamins reflects their intake in humans. However, some have reported that physical characteristics and urine volume may affect the amount of vitamin compounds found in urine. We hypothesized that physical characteristics and urine volume could affect urinary excretion of B-group vitamins. Twenty-four-hour urine samples were collected from 186 free-living Japanese women aged 19 to 21 years and 104 free-living Japanese subjects aged 70 to 84 years. Correlations between urinary output of each B-group vitamin and body height, body weight, body mass index, body surface area, urine volume, and urinary creatinine were determined. Only urinary vitamin B(12) was strongly correlated to urine volume in young (r = 0.683, P < .001) and elderly (r = 0.523, P < .001) subjects. To confirm this finding, 20 Japanese adults were orally administered 1.5 mg of cyanocobalamin (500-fold higher daily intake); and correlations between urinary vitamin B(12) and urine volume were determined. The load of cyanocobalamin increased vitamin B(12) content in the urine by only 1.3-fold. Urinary vitamin B(12) was strongly correlated with urine volume on the day before taking, the day of taking, and the day after taking cyanocobalamin (r = 0.745, P < .001; r = 0.897, P < .0001; and r = 0.855, P < .0001, respectively). We conclude that urinary excretion of vitamin B(12) is dependent upon urine volume, but not on intake of vitamin B(12). Physical characteristics and urine volume are less important for B-group vitamins except for vitamin B(12) as biomarker.

ABSORPTION and excretion of vitamin B12 in rats and man.

ABSORPTION and excretion of vitamin B12 in rats and man.

Urinary Excretion of Vitamin B12 in Human Beings

Urinary Excretion of Vitamin B12 in Human Beings

SERUM concentration and urinary excretion of vitamin B12.

Serum Concentration and Urinary Excretion of Vitamin B12 Get access Nutrition Reviews, Volume 12, Issue 4, April 1954, Pages 105–107, https://doi.org/10.1111/j.1753-4887.1954.tb03218.x Published: 01 April 1954

Pharmacokinetics of high doses of cyanocobalamin administered by i.v. injection in healthy volunteers

In order to evaluate the pharmacokinetics of high doses of Vitamin B12, 20 healthy subjects were randomly allocated into 5 equal groups to intravenously receive a single dose of 1 mg, 10 mg, 25 mg, 100 mg, and 300 mg of Vitamin B12, respectively. A noncompartmental analysis (WinNonlin) followed by a population two-compartmental analysis (P-Pharm) was performed. Plasma and urine levels of vitamin B12 were quantified by HPLC (detection limit: 30 ng/ml). The plasma levels of 1 mg of Vitamin B12 were not detected. An increase from 10 mg to 25 mg to 100 mg to 300 mg resulted in a proportional increase of Cmax. The fractional AUC and AUC0-Inf increased proportional to the doses. The half life was between 1.5 to 2.1 h, with no effect of the dose. The Cl and Vdss showed a tendency to increase at a rate quite lower than the increase in dose. The population Cl, Vdss, and kel were similar to those derived from the noncompartment analysis. The urinary excretion of Vitamin B12 increased with dose, being excreted >75% of 10 mg in 24 hours. In conclusion, the PK profile of large single doses of Vitamin B12 intravenously administered is linear in a range between 10 to 300 mg and is properly described by a two-compartment PK model. Clinical Pharmacology & Therapeutics (2004) 75, P84–P84; doi: 10.1016/j.clpt.2003.11.321

Familial selective vitamin B12 malabsorption (Imerslund-Gräsbeck syndrome) in a pool of Turkish patients.

Thirty-six patients with Imerslund-Gräsbeck syndrome are presented. The mean ages at presentation and diagnosis were 4.7 +/- 3.7 years and 7.2 +/- 4.2 years, respectively. The mean hemoglobin level was 5.8 +/- 2.2 g/dL, the mean cell volume was 104.9 +/- 11.6 fL, the white blood cell count was 4479 +/- 2022/mm3, and the serum vitamin B12 level was 96.9 +/- 73 pg/mL. At diagnosis, 5 of the 36 patients, aged 5 to 16 years, had neurologic symptoms. All the patients had severe megaloblastic changes in bone marrow precursor cells. Proteinuria was detected in 78% of them. Patients with proteinuria had a younger age of onset (P < 0.0001) and diagnosis (P < 0.001) compared with those without proteinuria. In all patients, vitamin B12 excretion unbound to intrinsic factor after a flushing dose of vitamin B12 was lower than normal, and there was no appreciable correction in urinary vitamin B12 excretion after binding of intrinsic factor. The impairment of vitamin B12 absorption studies in Schilling tests; however, showed great variation among patients. Serum haptoglobin values were close to zero in all patients, indicating the presence of that intravascular hemolysis in Imerslund-Gräsbeck syndrome. Variations among patients in the age of presentation, degree of impairment of vitamin B12 absorption, and presence or absence of proteinuria suggest a heterogeneity in etiology of Imerslund-Gräsbeck syndrome at the molecular level.

The Value of Urine Creatinine Analysis in the Evaluation of Schilling Tests

We performed a prospective study to assess the clinical value of evaluating the adequacy of 24-hour urine specimens submitted for Schilling tests. A total of 121 specimens were evaluated of which 51 had abnormal vitamin B12 excretion values. Of those 51, there were 23 with apparently inadequate total creatinine content (implying a collection of less than 24 hours). Six of 12 specimens with less than 600 ml had adequate total creatinine content as well as normal vitamin B12 excretion. Compared with evaluation of specimen volume alone, these data support the inexpensive urine creatinine assay as a valuable source of information regarding the adequacy of 24-hour urine collections thereby improving the specificity of the Schilling test.

The influence of serum folate on urinary excretion of vitamin B12.

It was found that in patients with decreased serum folate concentration, urinary excretion of vitamin B12 was increased in a statistically highly significant way with both oral administration of 58 Co-labeled vitamin B12 and with a 57Co-labeled vitamin B12 intrinsic factor complex. This increased vitamin B12 excretion may account for some false normal Schilling test results. Furthermore, in folate deficiency, the intrinsic factor no longer seems required for vitamin B12 to pass the intestinal wall. It is also questionable whether vitamin B12 absorbed through the intestine under these circumstances could be properly metabolized. Besides statistical evidence, some clinical support for this theory is presented. These findings offer a possible clue for some literature reports that have lacked a satisfactory explanation.

Urinary oxalate excretion related to ileocolic surgery in patients with Crohn's disease.

Urinary oxalate excretion was studied in healthy subjects and before and after surgery in patients with Crohn's disease. Urinary oxalate excretion in relation to the length of diseased or resected ileal segment in patients subjected to restorative and colectomy procedures, as well as in relation to faecal excretion of fat and bile salts and to urinary excretion of vitamin B12 and calcium, was also studied. The studies were performed in patients on a free diet or standard hospital diet and on a high-oxalate and/or high-fat diet. When patients subjected to ileal resection in conjunction with minor colonic resection were studied on a high-oxalate diet, urinary oxalate excretion increased with length of ileum resected and correlated with faecal fat excretion and urinary excretion of vitamin B12 but not with faecal excretion of bile salts. Increasing the dietary fat intake in these patients further increased urinary oxalate excretion. Although urinary oxalate excretion increased somewhat in colectomized patients on a high-oxalate diet, indicating an increased absorption of dietary oxalate, this increase showed no correlation either to faecal fat or bile salt excretion, or to urinary excretion of vitamin B12. The result are consistent with the "solubility theory". A diet low in fat and oxalate and high in calcium is recommended in patients with hyperoxaluria.

Methylmalonic Acid and Vitamin B12 Excretion of Rats Consuming Diets Varying in Cellulose and Pectin

Methylmalonic Acid and Vitamin B12 Excretion of Rats Consuming Diets Varying in Cellulose and Pectin

Heterogeneity of hepatic vitamin B12 in the rat after parenteral cyanocobalamin.

1. The rate of radioactive vitamin B12 excretion into plasma and bile from the isolated perfused rat liver and into bile in vivo has been measured after the intramuscular injection of radioactive cyanocobalamin at various time-intervals before study. 2. With an interval of labelling of 10 or more days, the release of radioactive vitamin B12 over 4 h by the isolated perfused liver was linear and constituted approximately 3-5% and 1% of the hepatic radioactivity into plasma and bile respectively. 3. In contrast, after a shorter period of prelabelling (less than 7 days), there was a biphasic release of radioactive vitamin B12: an initial rapid rate followed by a slower rate after about 1 h of perfusion. The total radioactive vitamin B12 was considerably increased (e.g. 25% and 5% of hepatic radioactivity into plasma and bile respectively during a 4 h perfusion of a liver labelled 18 h previously). Confirmation of coexisting stable and labile pools of intrahepatic vitamin B12 was provided by: (a) the patterns of hepatic release after double labelling with 57Co-labelled and 58Co-labelled cyanocobalamin at different times before liver perfusion; (b) the rates of biliary excretion of 57Co-labelled and 58Co-labelled vitamin B12 in vivo after different periods of prelabelling. 5. The rate and pattern of release were not altered by changes in the quantity of precursor cyanocobalamin, by phenobarbitone treatment or by the addition of cycloheximide to the perfusion. 6. The injection into rats of subcellular preparations of rat liver labelled in vivo with radioactive vitamin B12 demonstrated that hepatic heterogeneity did not depend on physical compartmentation. 7. Despite the rapid release rate from the liver of recently administered radioactive cyanocobalamin, the hepatic radioactivity increased progressively with time after labelling in vivo, in contrast to the other tissues, where it decreased. In the presence of rapid bidirectional fluxes the ability of the liver to store vitamin B12 can be largely explained by the reduction in the rate of hepatic release that continues for about 10 days after parenteral administration of cyanocobalamin.

May the Schilling test be already repeated the next day using intrinsic factor?

The effect of previous administration of a dose of 1000 mu-g vitamin B12 on the Schilling test was examined in 18 patients, repeating the test 24 hrs later. On the first day 57-Co was administered, while on the second day 58-Co labeled vitamin B12 was given. The counting error was less than 2.0% at the 95% confidence level. A decrease in urinary excretion of vitamin B12 of 28.7 plus or minus 22.2% (x plus or minus SD) was found. The mean difference between the two subsequent Schilling test series was statistically significant (p less than 0.05). The excretion data of the first and the second test correlate well (r = 0.86; p less than 0.01; y = 0.66 x + 1.09). Thus the repeated Schilling test with intrinsic factor must not be performed the next day.

Vitamin B12 and vegetarianism in india.

Apparently healthy Indian lactovegetarians have significantly lower serum levels and urinary excretion of vitamin B12 as compared to non-vegetarians. The low levels of serum vitamin B12 in lactovegetarians are not due to defective absorption but to low dietary intake of this vitamin. Inspite of considerably low serum vitamin B12 values, the lactovegetarians have no apparent signs or symptoms of vitamin B12 deficiency and their response to injected cyanocobalamin mixed with tracer radioactive B12, as judged by urinary excretion pattern and liver uptake, was similar to that observed in nonvegetarians.

Radioactive Vitamin B12 Absorption Studies: Comparison of the Whole-Body Retention, Urinary Excretion, and Eight-hour Plasma Levels of Radioactive Vitamin B12

Abstract This paper reports the results of investigations designed to compare the whole-body retention, urinary excretion, and 8-hr plasma level of 58Co vitamin B12 in some 80 absorption tests on 50 subjects. Residual levels of radioactivity in the body were measured using a whole-body counter. A proportional relationship is demonstrated between the 9-day whole-body retention, the 8-hr plasma radioactivity and the 48-hr urinary excretion of vitamin B12. The constants of proportionality are determined, enabling the results of absorption tests carried out by different methods to be compared. The mean values and the range of the results obtained are tabulated for subjects in each of four clinical categories. It is shown that approximately one third of the activity absorbed from a 1-µg dose is excreted in the urine following a single intramuscular injection of 1 mg nonradioactive vitamin B12 at 3 hr. The administration of this flushing dose does not significantly alter the activity absorbed as represented by that retained together with that excreted in the urine. The plasma activity at 8 hr is increased by a factor of about 2 over that obtained without the flushing dose. Factors affecting the accuracy of the individual techniques have been studied and the poor reproducibility of successive tests is discussed.

Vitamin B12 excretion in patients with various skin diseases.

The excretion in the urine of (58)Co after an oral dose of (58)Co vitamin B(12) given together with intrinsic factor has been found to be reduced in a number of patients with psoriasis, eczema, and other less common dermatoses. There is a correlation between the abnormality and the extent of the rash. A reduced glomerular filtration rate was found in a few of the patients in whom it was measured, and this must have been responsible, at least in part, for the reduced excretion of vitamin B(12) in these patients, but abnormal vitamin B(12) excretion also occurred in the absence of impaired renal function. Our evidence is insufficient to show whether malabsorption or increased tissue utilization of vitamin B(12) was the explanation in other cases. Certainly a number of patients had steatorrhoea, and in these it is most likely that malabsorption was the major factor. In patients without steatorrhoea a lone malabsorption of vitamin B(12) cannot be excluded. A decreased serum concentration of vitamin B(12) was found in only one of the patients.

Vitamin B 12 excretion by the rat small intestine.

Two phases of intestinal excretion are demonstrated after a parenteral dose of (58)Co vitamin B(12). The first phase was maximal immediately after injection, and was related to plasma radioactivity. The second phase was delayed 36 to 48 hours and was related to labelled cells reaching the tips of the villi. The loss of vitamin B(12) through increased exudation and rapid cell exfoliation together with failure of reabsorption may play a part in the deficiency state seen in the coeliac syndrome.

Vitamin B12 binding proteins in liver disease.

Summary:Vitamin B12 binding proteins were studied in patients with acute and chronic liver disease, and compared with vitamin B12 binders in chronic myeloid leukemia.In acute viral hepatitis marked elevation of serum vitamin B12 was common. Although the serum vitamin B12 rose as high as that found in chronic myeloid leukaemia the unsaturated vitamin B12 binding capacity (UBBC) was markedly elevated in the latter condition, whereas it was decreased in acute liver disease. In cirrhosis a moderate increase of serum vitamin B12 and UBBC was common.Urinary vitamin B12 excretion increased significantly only when the serum vitamin B12 became markedly elevated in hepatitis.As in chronic myeloid leukaemia the alpha‐globulin vitamin B12‐binder carried the bulk of the elevated serum vitamin B12 in acute liver disease; the beta‐globulin vitamin B12‐binder was decreased in serum but seemed to be the predominant binder in urine. This suggests that renal loss of beta‐globulin binder is greater than renal loss of alpha‐globulin binder. Only minor albumin binding of vitamin B12 in liver disease was found in spite of marked elevation of the serum vitamin B12 level. In cirrhosis the serum alpha‐globulin binder was often increased and beta‐globulin binder decreased. The cause and significance of these findings are discussed.The ability of serum vitamin B12‐binders of liver disease to ‘transfer’57Co‐B12 to tissue was investigated in an in vitro rat liver homogenate system. In a limited study, vitamin B12 uptake appeared to be within normal limits, except for suboptimal uptake from the beta‐globulin binder in cirrhotic serum. Poor vitamin B12 uptake from chronic myeloid leukaemia serum (in particular alpha‐globulin binder) was confirmed.

Effects of smoking on metabolism and excretion of vitamin B12.

Effects of smoking on metabolism and excretion of vitamin B12.

Validity of the Assumption of Tracer Equilibrium with respect to the Excretion of Vitamin B12

Evidence apparently refuting the assumption of tracer equilibrium shortly after administration of vitamin B12 has been critically examined. It is fundamentally impossible to demonstrate differences between the excretion rate of labelled B12 and unlabelled B12 in the studies described. The apparent changes in the excretion rate of B12 are shown to be due to the pooling of data from several patients. The excretion data from whole-body monitoring of individual patients can be adequately described by a single exponential term, if the data from the first few days after administration are not considered. For a single pool system, the assumption of tracer equilibrium is justified. It is shown that excretion rates, calculated on the assumption of tracer equilibrium, agree with those estimated from independent clinical findings based on the time required to develop symptoms of hypovitaminosis following total gastrectomy. The data which dispute the assumption lead to excretion rates which are almost certainly underestimates.