scholarly journals Vitamin B12 deficiency results in the abnormal regulation of serine dehydratase and tyrosine aminotransferase activities correlated with impairment of the adenylyl cyclase system in rat liver

2008 ◽  
Vol 99 (3) ◽  
pp. 503-510 ◽  
Author(s):  
Shuhei Ebara ◽  
Motoyuki Nakao ◽  
Mayuko Tomoda ◽  
Ryoichi Yamaji ◽  
Fumio Watanabe ◽  
...  
Keyword(s):  
Adenylyl Cyclase ◽  
Rat Liver ◽  
Vitamin B12 Deficiency ◽  
Tyrosine Aminotransferase ◽  
Vitamin B ◽  
Deficient Diet ◽  
Adenylyl Cyclase System ◽  
Serine Dehydratase ◽  
B12 Deficiency ◽  
Induced Changes

The aim of the present study was to elucidate the mechanism of the vitamin B12 deficiency-induced changes of the serine dehydratase (SDH) and tyrosine aminotransferase (TAT) activities in the rat liver. When rats were maintained on a vitamin B12-deficient diet, the activities of these two enzymes in the liver were significantly reduced compared with those in the B12-sufficient control rats (SDH 2·8 (sd 0·56) v. 17·5 (sd 6·22) nmol/mg protein per min (n 5); P < 0·05) (TAT 25·2 (sd 5·22) v. 41·3 (sd 8·11) nmol/mg protein per min (n 5); P < 0·05). In the B12-deficient rats, the level of SDH induction in response to the administration of glucagon and dexamethasone was significantly lower than in the B12-sufficient controls. Dexamethasone induced a significant increase in TAT activity in the primary culture of the hepatocytes prepared from the deficient rats, as well as in the cells from the control rats. However, a further increase in TAT activity was not observed in the hepatocytes from the deficient rats, in contrast to the cells from the controls, when glucagon was added simultaneously with dexamethasone. The glucagon-stimulated production of cAMP was significantly reduced in the hepatocytes from the deficient rats relative to the cells from the control rats. Furthermore, the glucagon-stimulated adenylyl cyclase activity in the liver was significantly lower in the deficient rats than in the controls. These results suggest that vitamin B12 deficiency results in decreases in SDH and TAT activities correlated with the impairment of the glucagon signal transduction through the activation of the adenylyl cyclase system in the liver.

scholarly journals Cobalamin (vitamin B12)-deficiency-induced changes in the proteome of rat cerebrospinal fluid

2003 ◽  
Vol 374 (1) ◽  
pp. 239-246 ◽  
Author(s):  
Elisabetta GIANAZZA ◽  
Daniela VEBER ◽  
Ivano EBERINI ◽  
Francesca R. BUCCELLATO ◽  
Elena MUTTI ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
De Novo ◽  
Vitamin B12 Deficiency ◽  
Cobalamin Deficiency ◽  
Deficient Diet ◽  
Central Nervous System Damage ◽  
Replacement Treatment ◽  
B12 Deficiency ◽  
Specific Increase ◽  
Induced Changes

We studied the changes in the proteome of CSF (cerebrospinal fluid) in two animal models of Cbl (cobalamin) deficiency: TGX (totally gastrectomized) rats and rats fed a Cbl-D (Cbl-deficient) diet. Two-dimensional PAGE was used to detect qualitative and quantitative variations in proteins in the CSF samples. The peak increase in total CSF protein concentration was observed 4 months after TG (total gastrectomy) and after 6 months of eating a Cbl-D diet. There is a specific increase 4 months after TG in the spots corresponding to α1-antitrypsin and the de novo presence of thiostatin and haptoglobin β. Cbl-replacement treatment in 4-month-TGX rats corrected these alterations in the CSF proteome. However, most of the CSF proteome alterations attenuated in Cbl-untreated 8-month-TGX rats and in rats fed a Cbl-D diet for 16 months. Transthyretin concentration varied slightly in the CSF of both types of Cbl-D rat, whereas the relative abundance of prostaglandin D synthase rose sharply in the CSF of the rats fed a Cbl-D diet for 16 months. We have demonstrated previously that the histological and ultrastructural CNS (central nervous system) damage in both types of Cbl-D rat appears within 2–3 months of Cbl deficiency, and thus appears to precede the alterations in the CSF proteome. The CSF proteome patterns of rats in which phlogosis was induced in or outside the CNS are quite different from those of the CSF of Cbl-D rats. All these findings demonstrate that the alterations in the CSF proteome of Cbl-D rats are specifically linked to Cbl deficiency.

scholarly journals Some metabolic aspects of vitamin B12 deficiency in sheep

1970 ◽  
Vol 24 (4) ◽  
pp. 879-891 ◽  
Author(s):  
R. M. Smith ◽  
H. R. Marston
Keyword(s):  
Body Weight ◽  
Energy Metabolism ◽  
Nitrogen Metabolism ◽  
Vitamin B12 Deficiency ◽  
Vitamin B ◽  
Weight Changes ◽  
Body Weight Changes ◽  
Deficient Diet ◽  
Faecal Nitrogen ◽  
B12 Deficiency

1. Studies were made with pair-fed vitamin B12-deficient and vitamin B12-treated or cobalt-treated ewes fed a Co-deficient diet in cages. Measurements were made of body-weight changes and some observations were made of energy and nitrogen metabolism. The effects of oral Co on energy and nitrogen metabolism were examined in sheep fed the Co-deficient diet, but not yet deficient of vitamin B12 in the tissues.2. The rate of loss of body-weight of vitamin B12-deficient sheep was significantly faster (P<0.01) than that of pair-fed sheep given 50 μg vitamin B12/d by injection.3. In a limited number of observations of pair-fed sheep no significant differences were found in retention of combustible energy from the diet, but excretion of faecal nitrogen was higher in deficient animals than in animals receiving vitamin B12 or Co.4. There was no significant effect of supplementary Co on energy metabolism, nitrogen metabolism, production of methane or digestibility of fodder in sheep that were not deficient of vitamin B12.

scholarly journals Assessment of vitamin B12 deficiency and B12 screening trends for patients on metformin: a retrospective cohort case review

2021 ◽  
pp. bmjnph-2020-000193
Author(s):  
Darby Martin ◽  
Jeet Thaker ◽  
Maria Shreve ◽  
Lois Lamerato ◽  
Kartazyna Budzynska
Keyword(s):  
Retrospective Cohort ◽  
Protective Factor ◽  
Vitamin B12 Deficiency ◽  
Older Age ◽  
Secondary Outcome ◽  
Vitamin B ◽  
Case Review ◽  
Large Hospital ◽  
Hospital System ◽  
B12 Deficiency

ObjectivesOur study investigated the use of vitamin B12 testing in a large cohort of patients on metformin and assesses appropriateness and benefits of screening recommendations for vitamin B12 deficiency.DesignThis retrospective cohort study included insured adult patients who had more than 1 year of metformin use between 1 January 2010 and 1 October 2016 and who filled at least two consecutive prescriptions of metformin to establish compliance. The comparison group was not exposed to metformin. Primary outcome was incidence of B12 deficiency diagnosed in patients on metformin. Secondary outcome was occurrence of B12 testing in the patient population on metformin. Records dated through 31 December 2018 were analysed.SettingLarge hospital system consisting of inpatient and outpatient data base.ParticipantsA diverse, adult, insured population of patients who had more than 1 year of metformin use between 1 January 2010 and 1 October 2016 and who filled at least two consecutive prescriptions of metformin.ResultsOf 13 489 patients on metformin, 6051 (44.9%) were tested for vitamin B12 deficiency, of which 202 (3.3%) tested positive (vs 2.2% of comparisons). Average time to test was 990 days. Average time to test positive for deficiency was 1926 days. Factors associated with testing were linked to sex (female, 47.8%), older age (62.79% in patients over 80 years old), race (48.98% white) and causes of malabsorption (7.11%). Multivariable logistic regression showed older age as the only factor associated with vitamin B12 deficiency, whereas African-American ethnicity approached significance as a protective factor.ConclusionsBased on our study’s findings of vitamin B12 deficiency in patients on metformin who are greater than 65 years old and have been using it for over 5 years, we recommend that physicians consider screening in these populations.

Vitamin B12 deficiency is the dominant nutritional cause of hyperhomocysteinemia in a folic acid-fortified population

2005 ◽  
Vol 43 (10) ◽  
Author(s):  
Ralph Green ◽  
Joshua W. Miller
Keyword(s):  
United States ◽  
Folic Acid ◽  
Vitamin B12 Deficiency ◽  
The United States ◽  
Community Dwelling ◽  
Vitamin B ◽  
Prevalence Rates ◽  
Total Vitamin ◽  
Folic Acid Fortification ◽  
B12 Deficiency

AbstractPrevalence rates for folate deficiency and hyperhomocysteinemia have been markedly reduced following the introduction of folic acid fortification in the United States. We report the prevalence of hyperhomocysteinemia in a population of community-dwelling elderly Latinos in the post-folic acid fortification era. We measured homocysteine, total vitamin B

Ileocaecal tuberculosis: an under-recognised cause of vitamin B12 deficiency

2018 ◽  
Vol 49 (2) ◽  
pp. 143-144
Author(s):  
Ashok Kumar Pannu ◽  
Dinesh Raja Palanisamy
Keyword(s):  
Terminal Ileum ◽  
Vitamin B12 Deficiency ◽  
Abdominal Tuberculosis ◽  
Megaloblastic Anaemia ◽  
Vitamin B ◽  
Lower Quadrant ◽  
Abdominal Tenderness ◽  
B12 Deficiency ◽  
Clinical Triad ◽  
Right Lower Quadrant

A combination of anaemia and knuckle pigmentation should always raise concern for megaloblastic anaemia. As the terminal ileum is the site of vitamin B12 absorption and also the commonest site of abdominal tuberculosis, a clinical triad of prolonged fever, knuckle pigmentation and right lower quadrant abdominal tenderness should suggest ileocaecal tuberculosis in endemic areas.

Effects of vitamin B12 deficiency on lipid metabolism of the rat liver and nervous system

1978 ◽  
Vol 39 (3) ◽  
pp. 501-513 ◽  
Author(s):  
C. Fehling ◽  
Margaretha JÄgerstad ◽  
B. Åkesson ◽  
J. Axelsson ◽  
A. Brun
Keyword(s):  
Fatty Acids ◽  
Nervous System ◽  
Fatty Acid ◽  
Motor Nerve ◽  
Vitamin B12 Deficiency ◽  
Neurological Dysfunction ◽  
Vitamin B ◽  
Deficient Diet ◽  
Neurological Signs ◽  
The Central Nervous System

1. Rats bred from vitamin B12-depleted dams were fed on a vitamin B12-deficient diet for 12–15 months and developed a severe vitamin B12 deficiency, as judged from methylmalonic acid excretion and tissue vitamin B12 levels at slaughter. Control rats were supplemented with vitamin B12 in the drinking-water.2. Neurological signs were recorded after 7 months but the motor nerve conduction velocities remained normal. Neuropathological examination revealed mild changes in the peripheral nerves but no changes in the central nervous system.3. The amounts of total lipids and phospholipids were normal, but in all examined tissues the proportions of pentadecanoate (C15 fatty acid) and heptadecanoate (C17 fatty acid) were considerably increased in vitamin B12 deficiency.4. 3H2O was incorporated to the same extent into the fatty acids of nervous tissue from vitamin B12-deficient and control rats after 48 h. Less 3H was found in the liver fatty acids of the vitamin B12-deficient rats.5. Neurological dysfunction can be demonstrated in the vitamin B12-deficient rat; the relation of the biochemical and neuropathological changes to the neurological signs needs further study.

scholarly journals Improved testing for vitamin B12 deficiency: correcting MMA for eGFR reduces the number of patients classified as vitamin B12 deficient

2018 ◽  
Vol 55 (6) ◽  
pp. 685-692 ◽  
Author(s):  
Saskia LM van Loon ◽  
Anna M Wilbik ◽  
Uzay Kaymak ◽  
Edwin R van den Heuvel ◽  
Volkher Scharnhorst ◽  
...  
Keyword(s):  
Data Mining ◽  
Vitamin B12 ◽  
Methylmalonic Acid ◽  
Vitamin B12 Deficiency ◽  
The Elderly ◽  
Vitamin B ◽  
Data Mining Approach ◽  
Number Of Patients ◽  
B12 Deficiency ◽  
The Relationship

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.

scholarly journals Homocystinuria masquerading as vitamin B12 deficiency

2012 ◽  
Vol 4 (2) ◽  
pp. 326-328
Author(s):  
M Wadhwani ◽  
S Beri ◽  
A Saili ◽  
S Garg
Keyword(s):  
Vitamin B12 ◽  
Megaloblastic Anemia ◽  
Vitamin B12 Deficiency ◽  
Interesting Case ◽  
Vitamin B ◽  
Ophthalmological Examination ◽  
Ophthalmic Manifestations ◽  
History Of ◽  
B12 Deficiency ◽  
Vitamin B 12

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

scholarly journals The experimental production of vitamin B12 deficiency in the baboon (Papio cynocephalus). A 2-year study

1974 ◽  
Vol 32 (2) ◽  
pp. 219-228 ◽  
Author(s):  
R. C Siddons
Keyword(s):  
Methylmalonic Acid ◽  
Daily Intake ◽  
Serum Vitamin ◽  
Vitamin B12 Deficiency ◽  
Vegetarian Diet ◽  
Vitamin B ◽  
Papio Cynocephalus ◽  
Experimental Production ◽  
Deficient Diet ◽  
Liver Vitamin

1. The development of vitamin B12 deficiency, as indicated by the serum and liver vitamin B12 levels and the excretion of methylmalonic acid, was studied over a 2-year period in baboons (Papio cynocephalus) given a diet deficient in vitamin B12. The effects of partial hepatectomy and the inclusion of either ampicillin or sodium propionate in the diet on the rate of development of the deficiency were also studied.2. The baboons had previously been fed on a mainly vegetarian diet. Their serum vitamin B12 levels were less than 100 ng/l and the mean liver vitamin B12 concentration was 0·56 μ/g. Similar serum and liver vitamin B12 levels were found in baboons given a purified diet supplemented with 1 μg vitamin B12/d, and marked increases in the serum and liver vitamin B12 levels occurred when the daily intake was increased to 2 μg.3. The serum vitamin B12 levels decreased to less than 20 ng/l in all baboons given a vitamin B12-deficient diet.4. The liver vitamin B12 concentration also decreased in all baboons given a deficient diet. At 9 months the lowest levels (0·20 μ/g) were found in partially hepatectomized baboons but subsequently baboons given the diet containing ampicillin had the lowest levels (0·11 μ/g).5. The excretion of methylmalonic acid after a valine load was found to be inversely related to the liver vitamin B12 concentration. In the early part of the study, partially hepatectomized baboons excreted the highest amount but subsequently baboons given a diet containing ampicillin excreted the highest amount.6. Increased formiminoglutamic acid excretion after a histidine load was observed in two baboons given a vitamin B12-deficient diet and in both baboons the liver folic acid concentration was low.7. No haematological or neurological symptoms of the vitamin B12 deficiency were observed.

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