scholarly journals Effect of Vitamin B12 deficiency on phosphatidylethanolamine methylation in rat liver

1978 ◽  
Vol 40 (3) ◽  
pp. 521-527 ◽  
Author(s):  
B. Åkesson ◽  
C. Fehling ◽  
Margaretha JÄGerstad

1. In vitamin B12 deficiency the activity of tetrahydropteroylglutamate methyltransferase (EC 2.1.1.13) is depressed and the synthesis of methionine is reduced. Because the methyl group of methionine is largely utilized for the methylation of phosphatidylethanolamine, we investigated the effects of vitamin B12 deficiency on phosphatidylcholine synthesis.2. The incorporation of injected [14Clformaldehyde into liver phosphatidylcholine was reduced by approximately 50% in vitamin B12-deficient rats. Also the corresponding incorporation of 5-[14C]methyl-tetrahydrofolic acid tended to decrease. The findings are consistent with a lower conversion of these precursors to methionine.3. The effect of the deficient methyl-group supply on phosphatidylcholine synthesis was also investigated by the injection of [14C]ethanolamine. The amount (%) of lipid-14C recovered in phosphatidylcholine was significantly reduced in vitamin B12 deficiency.4. Chemical analysis of liver phospholipids showed that the vitamin B12-deficient rats had a higher proportion of phosphatidylethanolamine and a lower proportion of phosphatidylcholine, indicating that the impaired synthesis of phosphatidylcholine by methylation leads to changes in membrane phospholipid composition.

1974 ◽  
Vol 47 (6) ◽  
pp. 617-630
Author(s):  
A. Lavoie ◽  
E. Tripp ◽  
A. V. Hoffbrand

1. The uptake of 14C from [methyl-14C]methyItetrahydrofolate was significantly reduced in the phytohaemagglutinin (PHA)-stimulated lymphocytes from nine patients with untreated pernicious anaemia compared with the uptake in seven normal subjects. 2. The uptake of 14C from [14C]methyltetrahydrofolate by the lymphocytes from seven of the patients with pernicious anaemia was consistently increased by addition of vitamin B12in vitro. 3. The proportion of 14C taken up from [14C]methyltetrahydrofolate transferred to non-folate compounds was found to be significantly reduced in the PHA-stimulated lymphocytes from nine patients with untreated pernicious anaemia compared with the proportion transferred in the PHA-stimulated lymphocytes from seven normal subjects. Addition of vitamin B12in vitro consistently increased the transfer in vitamin B12-deficient cells but had no consistent effect in normal cells. 4. Normal and vitamin B12-deficient PHA-stimulated lymphocytes took up [3H]folic acid and after 72 h incubation converted this largely into pteroylpolyglutamate forms. 5. The proportion of labelled lymphocyte folate as pteroylpolyglutamate after incubation with [3H]folic acid was the same in vitamin B12-deficient as in normal lymphocytes and the proportion of pteroylpolyglutamates formed in vitamin B12-deficient lymphocytes was unaffected by addition of vitamin B12in vitro. 6. No radioactivity could be decteted in pteroylpolyglutamates after incubating normal PHA-stimulated lymphocytes with [14C]methyltetrahydrofolate for 72 h, suggesting that pteroylpolyglutamate forms of folate cannot be made directly from methyltetrahydrofolate. 7. These results are consistent with the ‘methyltetrahydrofolate trap’ hypothesis in vitamin B12 deficiency. It is suggested that reduced synthesis of pteroylpolyglutamates reported by others in vitamin B12-deficient cells may be secondary to the failure of removal of the methyl group from methyltetrahydrofolate rather than to a direct effect of vitamin B12 deficiency on the enzyme responsible for pteroylpolyglutamate synthesis. 8. Reduced entry of methyltetrahydrofolate into vitamin B12-deficient cells may be secondary to failure of conversion of this compound into tetrahydrofolate.


Author(s):  
Saskia LM van Loon ◽  
Anna M Wilbik ◽  
Uzay Kaymak ◽  
Edwin R van den Heuvel ◽  
Volkher Scharnhorst ◽  
...  

Background Methylmalonic acid (MMA) can detect functional vitamin B12 deficiencies as it accumulates early when intracellular deficits arise. However, impaired clearance of MMA from blood due to decreased glomerular filtration rate (eGFR) also results in elevated plasma MMA concentrations. Alternative to clinical trials, a data mining approach was chosen to quantify and compensate for the effect of decreased eGFR on MMA concentration. Methods Comprehensive data on patient’s vitamin B12, eGFR and MMA concentrations were collected ( n = 2906). The relationship between vitamin B12, renal function (eGFR) and MMA was modelled using weighted multiple linear regression. The obtained model was used to estimate the influence of decreased eGFR on MMA. Clinical impact was examined by comparing the number of patients labelled vitamin B12 deficient with and without adjustment in MMA. Results Adjusting measured MMA concentrations for eGFR in the group of patients with low-normal vitamin B12 concentrations (90–300 pmol/L) showed that the use of unadjusted MMA concentrations overestimates vitamin B12 deficiency by 40%. Conclusions Through a data mining approach, the influence of eGFR on the relation between MMA and vitamin B12 can be quantified and used to correct the measured MMA concentration for decreased eGFR. Especially in the elderly, eGFR-based correction of MMA may prevent over-diagnosis of vitamin B12 deficiency and corresponding treatment.


2012 ◽  
Vol 4 (2) ◽  
pp. 326-328
Author(s):  
M Wadhwani ◽  
S Beri ◽  
A Saili ◽  
S Garg

Background: Homocystinuria is a rare metabolic disorder charcterised by excess homocysteine in the urine. Vitamin B12 deficiency has diverse cutaneous, nervous and ophthalmic manifestations. Objective: To report a case of homocystinuria masquerading as vitamin B 12 deficiency. Case: We hereby are presenting an interesting case of a 4 year old boy who was being treated for Vitamin B 12 deficiency on the basis of history of delayed milestone, abdominal pain and hyperpigmentation of skin which was diagnosed as homocystinuria. Conclusion: It is important to carry out ophthalmological examination in every case of megaloblastic anemia if associated with blurring of vision and mental retardation.DOI: http://dx.doi.org/10.3126/nepjoph.v4i2.6554 Nepal J Ophthalmol 2012; 4 (8): 326-328


Author(s):  
Raquel Aparicio-Ugarriza ◽  
Gonzalo Palacios ◽  
Monika Alder ◽  
Marcela González-Gross

AbstractVitamin B


2020 ◽  
Vol 2 (8) ◽  
pp. 01-03
Author(s):  
Rateesh Sareen

Vitamin B12 assay is one of the most frequently ordered tests particularly as a part of regular medical checkups. The deficiency is rampant in vegetarian population. It is of immense importance that laboratories establish their own reference interval (RI) of analyte specially Vitamin B12 as a diagnosis of Vitamin B12 deficiency based on RI of kit insert inadvertently leads to unnecessary treatment or work up. A blind reliance on RI of kit insert should be discouraged as they do not take into account population characteristics and do not truly reflect RI specific to the population under study.


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.


1961 ◽  
Vol 200 (1) ◽  
pp. 99-101 ◽  
Author(s):  
B. L. O'Dell ◽  
B. A. Erickson ◽  
P. M. Newberne ◽  
L. M. Flynn

A vitamin B12 deficiency in weanling rats, which reduced their average weight to one-half that of controls, decreased liver concentration of nonprotein sulfhydryl (NPSH) compounds about 10% but had no effect on concentration of disulfide compounds. Fasting did not accentuate the effect of the deficiency. Dams severely depleted of B12 produced offspring whose livers contained significantly less NPSH and correspondingly more nonprotein disulfide (NPSS) compounds than controls. Thus the decreased concentration of NPSH on the B12-deficient liver was accounted for as NPSS. Vitamin B12 deficiency had no effect on the rate of anaerobic glycolysis in liver and brain tissues.


2015 ◽  
Vol 34 (4) ◽  
pp. 467-472 ◽  
Author(s):  
Anđelo Beletić ◽  
Duško Mirković ◽  
Aleksandra Dudvarski-Ilić ◽  
Branislava Milenković ◽  
Ljudmila Nagorni-Obradović ◽  
...  

SummaryBackground:An increased homocysteine (Hcy) concentration may represent a metabolic marker of folate and vitamin B12deficiency, both significant public health problems. For different reasons, patients with chronic obstructive pulmonary disease (COPD) are prone to these deficiencies. The study evaluates the reliability of Hcy concentration in predicting folate or vitamin B12deficiency in these patients.Methods:A group of 50 COPD patients (28 males/22 females, age$({\rm{\bar x}} \pm {\rm{SD}} = 49.0 \pm 14.5)$years was enrolled. A chemiluminescent microparticle immunoassay was applied for homocysteine, folate and vitamin B12concentration. Kolmogorov-Smirnov, Mann-Whitney U and χ2tests, Spearman’s correlation and ROC analysis were included in the statistical analysis, with the level of significance set at 0.05.Results:Average (SD) concentrations of folate and vitamin B12were 4.13 (2.16) μg/L and 463.6 (271.0) ng/L, whereas only vitamin B12correlated with the Hcy level (P=−0.310 (R=0.029)). Gender related differences were not significant and only a borderline significant correlation between age and folate was confirmed (R=0.279 (P=0.047)). The incidence of folate and vitamin B12 deficiency differed significantly (P=0.000 and P<0.000 for folate and vitamin B12respectively), depending on the cut-off used for classification (4.4, 6.6 and 8.0 μg/L – folate; 203 and 473 ng/L – vitamin B12). ROC analyses failed to show any significance of hyperhomocysteinemia as a predictor of folate or vitamin B12deficiency.Conclusion:Reliability of the Hcy concentration as a biomarker of folate or vitamin B12depletion in COPD patients is not satisfactory, so their deficiency cannot be predicted by the occurrence of HHcy.


2014 ◽  
Vol 04 (01) ◽  
pp. 104-105
Author(s):  
Prassanna Baby ◽  

Abstract:Vitamin B12 is a crystalline compound essential to a number of micro-organisms and animals, including humans. So far as is known it is not present in higher plants. Pure vegetarian food is nearly free from vit. B12. It is a nutrient that needs attention in vegan diet. Vegetarians are at risk for vitamin B(12) (B12) deficiency due to suboptimal intake. Dietary deficiency of vitamin B12 due to vegetarianism is increasing and causes hyperhomocysteinemia Areas for research include intermittent vitamin B12 supplement dosing and better measurements of the bioavailability of B12 in fermented vegetarian foods and algae. The goal of the present literature review was to create an awareness among the vegans to identify the vegetarian sources of Vitamin B12 and to incorporate them into their daily diet.


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.


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