Vitamin B12 by mouth

1966 ◽  
Vol 4 (22) ◽  
pp. 85-86

The small quantity of vitamin B12 in a normal diet is absorbed by a complex process involving the liberation of the vitamin from food proteins, its combination with a glycoprotein secreted by the gastric mucosa (‘intrinsic factor’), its uptake by the ileal mucosa and its transfer to the blood stream.1 Vitamin B12 in very large amounts, and probably some of that present in liver and kidney, is absorbed mainly by direct diffusion without the participation of intrinsic factor.

1969 ◽  
Vol 47 (6) ◽  
pp. 497-504
Author(s):  
R. M. Taylor ◽  
J. A. Hildes ◽  
J. F. Lind

The absorption of physiological amounts of vitamin B12 is thought to occur only from the ileum, but the nature of the mechanism involved has not been established. A method utilizing the detection of radioactive vitamin B12 in plasma was used to investigate the mechanism of vitamin B12 absorption in dogs with isolated Thiry–Vella loops of small intestine, either ileum or jejunum. An animal with a Thiry–Vella loop of the entire ileum failed to absorb orally administered vitamin B12, but did absorb the vitamin from the isolated ileal loop when it was given with intrinsic factor, but not when given without. Attempts to restore absorption of orally administered vitamin B12 by the administration of ileal juice (either resting or stimulated), by the administration of an extract of ileal mucosa, or by the simultaneous absorption of non-radioactive vitamin B12 from the ioslated loop, all failed. In contrast, the animal with a jejunal Thiry–Vella loop absorbed vitamin B12 given orally but not when administered into the isolated jejunum alone, in combination with intrinsic factor, or with intrinsic factor and ileal juice. Under the conditions of these experiments the results confirm that vitamin B12 absorption is limited to the ileum, but fail to provide support for the hypothesis that the ileum liberates, either locally or systemically, a vitamin B12 absorption factor. Thus the hypothesis that ileal mucosa contains a special cellular mechanism for vitamin B12 absorption gains indirect support from these results.


1965 ◽  
Vol 208 (1) ◽  
pp. 14-17 ◽  
Author(s):  
Kunio Okuda ◽  
Katsumi Sasayama

Evidence is presented that intrinsic-factor (IF) activity is present in the small intestine as far down as the ileal end. Physiologic doses of radioactive vitamin B12 without IF were applied directly into various levels of the intestine by surgical and other means in man and rats, and significant absorption was obtained from the small intestine. Absorption inhibition by ethylenediaminetetraacetate and its counteraction by Ca ion demonstrated that such absorption was dependent on IF action. The large intestine was shown to be incapable of physiologic absorption of vitamin B12, and IF was totally ineffective. It is proposed that physiologically, gastric IF descends with some activity in the small intestine, where more of the food vitamin B12 is liberated by digestion and subjected to IF.


PLoS ONE ◽  
2021 ◽  
Vol 16 (3) ◽  
pp. e0249325
Author(s):  
Samuel Asamoah Sakyi ◽  
Edwin Ferguson Laing ◽  
Richard Mantey ◽  
Alexander Kwarteng ◽  
Eddie-Williams Owiredu ◽  
...  

Background The association between prolong metformin usage and B12 deficiency has been documented. However, the prevalence estimates of metformin-induced vitamin B12 deficiency showed substantial disparity among studies due to varied study definitions of vitamin B12 deficiency. Metformin blocks the calcium dependent absorption of the vitamin B12-Intrinsic Factor complex at the terminal ileum. Lack of intrinsic factor due to the presence of auto-antibodies to parietal cells (IFA) could lead to vitamin B12 deficiency and subsequently cause peripheral neuropathy. We investigated the prevalence of vitamin B12 deficiency using more sensitive, combined markers of vitamin B12 status (4cB12) and the immuno-biochemical mediators of vitamin B12 deficiency. Methods In this observational study, 200 consecutive consenting metformin-treated T2DM patients, aged 35 and above, attending the diabetic clinic at KATH were recruited. Vitamin B12 deficiency was classified based on the Fedosov age-normalized wellness quotient. Anthropometric measurement was taken as well as blood samples for immunological and biochemical mediators. Peripheral neuropathy was assessed using the Michigan Neuropathy Screening Instrument (MNSI). Statistical analysis was performed using the R Language for Statistical Computing. Results Using the combined indicator (4cB12), the prevalence of metformin induced vitamin B12 deficiency was 40.5% whilst the prevalence of MNSI-Q and MNSI-PE diabetic neuropathy was 32.5% and 6.5% respectively. Participants with vitamin B12 deficiency had significantly higher levels of IFA, GPA, TNF-α, TC, LDL and albumin compared to those with normal vitamin B12 levels (p < 0.05). Correlation analysis revealed a statistically significant negative association between 4cB12 and the immunological markers [IFA (rs = -0.301, p<0.0001), GPA (rs = -0.244, p = 0.001), TNF-α (rs = -0.242, p = 0.001) and IL-6 (rs = -0.145, p = 0.041)]. Likewise, 4cB12 was negatively associated with TC (rs = -0.203, p = 0.004) and LDL (rs = -0.222, p = 0.002) but positively correlated with HDL (rs = 0.196, p = 0.005). Conclusion Vitamin B12 deficiency and diabetic neuropathy are very high among metformin-treated T2DM patients and it is associated with increased GPA, IFA, TNF-α and cardiometabolic risk factors (higher LDL and TC and lower HDL). Upon verification of these findings in a prospective case-control study, it may be beneficial to include periodic measurement of Vitamin B12 using the more sensitive combined indicators (4cB 12) in the management of patients with T2DM treated with metformin in Ghana.


1963 ◽  
Vol 204 (1) ◽  
pp. 97-100 ◽  
Author(s):  
Agna Boass ◽  
T. Hastings Wilson

The stimulation of vitamin B12 uptake by small segments of hamster ileum in the presence of gastric intrinsic factor (IF) has been utilized as a quantitative assay for rat and hamster IF. About 100–150 small segments of everted ileum of the hamster were mixed in a beaker and aliquots of approximately 10 were incubated in flasks containing radioactive B12 with or without IF. Within a certain range of IF concentrations, B12 uptake into the tissue was proportional to the IF added. Of all the tissues studied only gastric mucosa showed IF activity under these conditions. This assay was not only specific for gastric IF, but was also extremely sensitive, giving a positive reaction with a concentration of 0.1 mg gastric mucosa per milliliter of incubating solution.


2020 ◽  
Author(s):  
Samuel Sakyi ◽  
Edwin F. Laing ◽  
Richard Mantey ◽  
Alexander Kwarteng ◽  
Eddie-Williams Owiredu ◽  
...  

Abstract Background: The association between prolong metformin usage and B12 deficiency has been documented. However, the prevalence estimates of metformin-induced vitamin B12 deficiency showed substantial disparity among studies due to varied study definitions of vitamin B12 deficiency. Metformin blocks the calcium dependent absorption of the vitamin B12-Intrinsic Factor complex at the terminal ileum. Lack of intrinsic factor due to the presence of auto-antibodies to parietal cells (IFA) could lead to vitamin B12 deficiency and subsequently cause peripheral neuropathy. We investigated the prevalence of vitamin B12 deficiency using more sensitive, combined markers of vitamin B12 status (4cB12) and the immuno-biochemical mediators of vitamin B12 deficiency.Methods: In this observational study, 200 consecutive metformin-treated T2DM patients, aged 35 and above, attending the diabetic clinic at KATH were recruited. Vitamin B12 deficiency was classified based on the Fedosov age-normalized wellness quotient. Anthropometric measurement was taken as well as blood samples for immunological and biochemical mediators. Peripheral neuropathy was assessed using the Michigan Neuropathy Screening Instrument (MNSI). Statistical analysis was performed using the R Language for Statistical Computing version 3.6.0. Results: Using the combined indicator (4cB12), the prevalence of metformin induced vitamin B12 deficiency was 40.5% whilst the prevalence of MNSI-Q and MNSI-PE diabetic neuropathy was 67.5% and 93.5% respectively. Participants with vitamin B12 deficiency had significantly higher levels of IFA, GPA, TNF-α, TC, LDL and albumin compared to those with normal vitamin B12 levels (p < 0.05). Correlation analysis revealed a statistically significant negative association between 4cB12 and the immunological markers [AIF (rs= -0.301, p<0.0001), GPA (rs= -0.244, p=0.001), TNF-α (rs= -0.242, p=0.001) and IL-6 (rs= -0.145, p=0.041)]. Likewise, 4cB12 was negatively associated with TC (rs= -0.203, p=0.004) and LDL (rs= -0.222, p=0.002) but positively correlated with HDL (rs= 0.196, p=0.005).Conclusion: Vitamin B12 deficiency and diabetic neuropathy are very high among metformin-treated T2DM patients and it is associated with increased GPA, IFA, TNF-α and cardiometabolic risk factors (higher LDL and TC and lower HDL). It is imperative Ghana include routine measurement of Vitamin B12 deficiency using the more sensitive combined indicators (4cB12), in the management of T2DM patients on metformin.


2020 ◽  
Vol 3 (2) ◽  
pp. 01-04
Author(s):  
Asmaa Hamouda

Obesity is the most prevalent nutritional dysfunction in society and the vital risk determinant for several relevant disorders. The first step of obesity assessment is calculated anthropometric measures and, secondly, measure biological and nutritional profiles. The current purpose is to investigate the relationship between BMI with biochemical profile, Vitamin B12, Fe, and cortisol in the volunteer’s population. There is an appositively connection between body mass index (BMI) with cortisol, liver and kidney profile, fasting blood sugar (FBS), Cholesterol, triglyceride, and low-density lipoprotein (LDL) and negative relationship between BMI and Vitamin B12, Fe, and high-density lipoprotein (HDL) in the present study. There is a significant elevation of cortisol, lipid profile, FBS, liver, and kidney function with BMI in the current work in females more than males compared to a reference range, and a significant decrease in Fe and vitamin B that can be due to diet habits, BMI, malabsorption in obesity condition, hormones affect or genetic variations between male and female. That will need further investigation.


1960 ◽  
Vol 15 (1) ◽  
pp. 11-23 ◽  
Author(s):  
M. Staak ◽  
H. C. Heinrich

Die am Meerschweinchen durchgeführten Studien über den physiologischen Bereich und den zeitlichen Verlauf der intestinalen Vitamin B12-Resorption zeigen, daß im Bereich einer Testdosis von 10 ng bzw. 30 ng 60Co-B12 die absolute Leber-Inkorporation noch annähernd linear-proportional zur oralen Testdosis verläuft und sich bei einer Testdosis von 50 ng 60Co-B12 bereits der Übergang in den Sättigungsbereich deutlich abzeichnet. 4 Stdn. nach oraler Applikation einer B12-Testdosis von 30 ng erreicht die 60Co-B12-Inkorporation in den Dünndarm ihr Maximum und nimmt dann schnell ab, während die Leber-Inkorporation nach 8 Stdn. ein Plateau erreicht, das mit längerer Testdauer (bis 48 Stdn.) nur noch unwesentlich ansteigt. Resorptionsort ist beim Meerschweinchen das gesamte Intestinum, jedoch bevorzugt dessen distaler Abschnitt.Die intestinale Vitamin B12-Resorption des Meerschweinchens ist ebenfalls hochgradig strukturspezifisch. Das 5.6-Dimethylbenzimidazolcyanocobamid, das 5.6-Dichlorbenzimidazolcyanocobamid, das Benzimidazolcyanocobamid und das 5-Methoxybenzimidazolcyanocobamid werden fast in gleichem Ausmaß wie das Vitamin B12 resorbiert, während die Resorption des 5-Hydroxybenzimidazolcyanocobamids wesentlich geringer ist und für das 3.5.6-Trimethylbenzimidazolcyanocobamid und Dicyanocorphinamid keine oder nur eine minimale Resorbierbarkeit nachgewiesen werden konnte. Diese Ergebnisse stimmen mit den am Menschen und am Schwein erhaltenen Resultaten gut überein. Auf Grund der vorliegenden Untersuchungen am Meerschweinchen müssen für eine optimale Vitamin B12-Resorption folgende struktur-chemische Bedingungen im Vitamin B12-Molekül erfüllt sein:1. Das Vorhandensein einer Nucleotid-Seitenkette. Ferner muß die koordinative Bindung zwischen dem zentralen Co-Atom und dem Benzimidazolring des Vitamin B12-Moleküles intakt sein.2. Der Benzimidazolring des Vitamin B12-Moleküles darf in 5-Position nicht mit einer freien phenolischen Hydroxylgruppe substituiert sein. Verätherung der phenolischen OH-Gruppe des 5-Hydroxybenzimidazolcyanocobamids mit einer CH3-Gruppe beseitigt den Hemmungseffekt des Phenolhydroxyls.Die Ursache der Strukturspezifität der intestinalen Vitamin B12-Resorption wurde an Hand von radio-papierchromatographischen Untersuchungen diskutiert. Es wurde festgestellt, daß einer ausgesprochenen Strukturspezifität der intestinalen Vitamin B12-Resorption eine durchaus strukturunspezifische Bindungsfähigkeit von rohen und gereinigten Intrinsic Factor-Präparaten für die einzelnen Vitamin B12-Analoga gegenübersteht. Es kann daher angenommen werden, daß die Strukturspezifität der Resorbierbarkeit des Vitamin B12-Moleküles durch den eigentlichen an der Intestinal-Mucosazelle ablaufenden und noch weitgehend unbekannten Resorptionsmechanismus bedingt ist, dem dann eine hohe Spezifität in der Auswahl der angebotenen Vitamin B12-Strukturen zukommen müßte.


1959 ◽  
Vol 14 (1) ◽  
pp. 42-49 ◽  
Author(s):  
H. C. Heinrich ◽  
R. Skibbe ◽  
M. Staak

1. 10 g ʟ (-) Sorbose hemmen bei etwa einem Drittel der daraufhin mit Hilfe des Radio-B12-Urincxkretions-Testes untersuchten Menschen mit normaler Vitamin B12-Resorption die intestinale Resorption einer physiologischen Radio-Vitamin B12-Testdosis von 0,5 μg beträchtlich, während bei den verbleibenden zwei Dritteln entweder keine Beeinflussung der Vitamin B12-Resorption oder aber ein zwischen 20 und 50% liegender Anstieg der Radio-B12-Harnexkretion beobachtet wurde. Eine weitere Heraufsetzung der Sorbosedosis (bis auf 50 g) ist dann fast stets von einer Hemmung der Vitamin B12-Resorption begleitet.2. Heterologer Intrinsic Factor ist zumindestens teilweise in der Lage, den Inhibitoreffekt der Sorbose auf die intestinale Vitamin B12-Resorption beim Menschen zu kompensieren.3. Bei Patienten mit gestörter Vitamin B12-Resorption (perniciöse Anämie bzw. einheimische Sprue) hatten ʟ (-) Sorbose und ᴅ (-) Sorbit in Mengen von 0,1 - 1 g bzw. 10 g eine zwar sehr geringe aber dennoch deutlich fördernde Wirkung auf die Radio-B12-Resorption, die jedoch im Vergleich mit dem wesentlich stärkeren Effekt von 12 mg Intrinsic Factor-Konzentrat unbedeutend und für eine praktische Perniciosa-Therapie uninteressant ist.4. Auch bei normalen Schweinen und Meerschweinchen wird die intestinale Resorption physiologischer Radio-B12-Testdosen von 0,5 μg bzw. 30 ng durch 20 g bzw. 100 mg ʟ (-) Sorbose stark gehemmt, wie mit dem Faeces- und Urinexkretions-Test bzw. mit dem Leberinkorporations-Test durchgeführte Untersuchungen ergaben.5. Der mögliche Wirkungsmechanismus des Sorbose-Hemmeffektes auf die intestinale Vitamin B12-Resorption beim Menschen, Schwein und Meerschweinchen wird auf Grund der schon unter in vitro-Bedingungen papierchromatographisch nachgewiesenen Bildung eines Sorbose-Vitamin B12- bzw. Sorbit-Vitamin B12-Komplexes diskutiert.


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