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.

scholarly journals Vitamin B12 nutrition and metabolism in the baboon (Papio cynocephalus)

1975 ◽  
Vol 33 (3) ◽  
pp. 415-424 ◽  
Author(s):  
R. C. Siddons ◽  
Fredericka Jacob
Keyword(s):  
Small Intestine ◽  
Oral Dose ◽  
Binding Capacity ◽  
Serum Vitamin ◽  
Middle Part ◽  
Dietary Vitamin ◽  
Vitamin B ◽  
Papio Cynocephalus ◽  
Significant Difference ◽  
Liver Vitamin

1. Measurement of the vitamin B12 content of baboon tissues showed that the liver contained the highest concentration, followed by the pituitary, kidney, heart, spleen and pancreas.2. The dietary vitamin B12 requirement of the baboon for the maintenance of satisfactory body stores was between 1 and 2 μg/d.3. Satisfactory liver vitamin B12 stores were invariably associated with serum levels above 125 pg/ml, whereas liver levels were usually low when the serum level was below 50 pg/ml.4. Increased methylmalonic acid (MMA) excretion after a valine load occurred when the liver vitamin B12 level was less than 0·40 μg/g. L- and DL-valine were approximately equally effective as precursors of MMA, whereas sodium propionate, whether given orally or intra-peritoneally, was less effective.5. The distribution of radioactivity along the wall of the intestinal tract after an oral dose of [57Co]cyanocobalamin suggested that the distal half of the small intestine was the main site of vitamin B12 absorption. However, the utilization of vitamin B12 put direct into the middle part of the small intestine was much lower than that of an oral dose.6. The unsaturated vitamin B12-binding capacity of baboon serum was not related to the serum vitamin B12 level. There was a significant difference between the unsaturated vitamin B12-binding capacities of the two subspecies of baboon (Papio cynocephalus cynocephalus and P. cynocephalus anubis) studied.

Serum Vitamin B12 Concentrations among Mothers and Newborns and Follow-up Study to Assess Implication on the Growth Velocity and the Urinary Methylmalonic Acid Excretion

2009 ◽  
Vol 79 (56) ◽  
pp. 297-307 ◽  
Author(s):  
Laila Hussein ◽  
Sahar Abdel Aziz ◽  
Salwa Tapouzada ◽  
Boehles
Keyword(s):  
Early Diagnosis ◽  
Growth Velocity ◽  
Methylmalonic Acid ◽  
Post Partum ◽  
Serum Vitamin ◽  
Vitamin B ◽  
Postnatal Life ◽  
Negative Consequences ◽  
Metabolic Marker ◽  
Biochemical Measurement

Objective:Cobalamin (B12) deficiency has been reported in infants born to mothers with low cobalamin intake. Early diagnosis of vitamin B12 deficiency in infants is critical for the prevention of neurobehavioral disorders. We investigated the relationship between serum vitamin B12 level in newborns and in their healthy mothers who consumed an omnivorous diet. Anthropometry was studied longitudinally to assess the growth velocity of the infants. Urinary methylmalonic acid (MMA) excretion of 6-month old infants was compared retrospectively as the biomarker correlated with the initial serum vitamin B12 concentrations. Methods: Serum cobalamin and blood hemoglobin were determined in 84 pairs of newborns and their mothers. Urinary MMA excretion was measured in the same subjects during the first 6 months of the post partum period. Results: At birth, median serum cobalamin levels were 152.0 pmol/L in the mothers and 296.6 pmol/L in the newborns. Maternal and neonatal serum cobalamin levels had no effect on growth velocity during the first six months of postnatal life. Serum maternal and neonatal cobalamin levels were inversely associated with urinary MMA excretion. Conclusion: Early diagnosis of vitamin B12 status in neonates and infants is crucial, particularly in nutritionally deprived areas. Biochemical measurement of plasma cobalamin or its metabolic marker MMA is highly recommended. Urinary MMA measurement in cobalamin diagnostics provides an advantage in that blood sampling is not required. A vitamin B12 taskforce should be created to alleviate vitamin deficiency and its negative consequences.

Effects of cobalt deficiency in the pregnant ewe on neonatal lamb survival

1992 ◽  
Vol 15 ◽  
pp. 169-171 ◽  
Author(s):  
G. E. J. Fisher ◽  
A. MacPherson
Keyword(s):  
Reproductive Performance ◽  
Dry Matter ◽  
Methylmalonic Acid ◽  
Milk Powder ◽  
Vitamin B ◽  
Deficient Diet ◽  
Cobalt Deficiency ◽  
Acid Status ◽  
Pregnant Ewe ◽  
Skimmed Milk Powder

It has been suggested (Mills, 1981) that there was a lack of research on the effects of cobalt (Co) deficiency on the reproductive performance of sheep. Duncan, Morrison and Garton (1981) reported that clinically Co-deficient ewes produced fewer lambs with a higher incidence of stillbirths and neonatal mortalities than Co-sufficient animals. Garton, Duncan and Fell (1981) related these findings to the vitamin B12 and methylmalonic acid status of dams. However, their investigations used few animals and were therefore inconclusive. The objectives of this work were to investigate the effects of subclinical Co deficiency in pregnant hill sheep on reproductive performance and neonatal lamb viability.Experiment 1 (1985/86) comprised 60 Scottish Blackface × Swaledale ewes, while experiment 2 (1986/87) included 30 of these animals plus 30 pure Scottish Blackface sheep. In both experiments the ewes were housed and bedded on sawdust and a Co-deficient diet of timothy hay, micronized maize, maize gluten, dibasic calcium phosphate and sodium chloride was offered. Skimmed milk powder was introduced to the diet during lactation. The Co content of the diet was 0.06 mg Co per kg dry matter.

scholarly journals Vitamin B12 status, cognitive decline and dementia: a systematic review of prospective cohort studies

2012 ◽  
Vol 108 (11) ◽  
pp. 1948-1961 ◽  
Author(s):  
Fiona O'Leary ◽  
Margaret Allman-Farinelli ◽  
Samir Samman
Keyword(s):  
Systematic Review ◽  
Cohort Studies ◽  
Cognitive Decline ◽  
Quality Assessment ◽  
Prospective Cohort ◽  
Methylmalonic Acid ◽  
Serum Vitamin ◽  
Assessment Tools ◽  
Vitamin B ◽  
Prospective Cohort Studies

Poor vitamin B12 status may lead to the development of cognitive decline and dementia but there is a large variation in the quality, design of and results reported from these investigations. We have undertaken a systematic review of the evidence for the association between vitamin B12 status and cognitive decline in older adults. A database search of the literature to 2011 was undertaken, using keywords related to vitamin B12 and cognition. All prospective cohort studies assessing the association of serum vitamin B12 or biomarkers were included. Quality assessment and extraction of the data were undertaken by two researchers. The quality assessment tool assigns a positive, neutral or negative rating. Of 3772 published articles, thirty-five cohort studies (n 14 325 subjects) were identified and evaluated. No association between serum vitamin B12 concentrations and cognitive decline or dementia was found. However, four studies that used newer biomarkers of vitamin B12 status (methylmalonic acid and holotranscobalamin (holoTC)) showed associations between poor vitamin B12 status and the increased risk of cognitive decline or dementia diagnosis. In general, the studies were of reasonable quality (twenty-one positive, ten neutral and four negative quality) but of short duration and inadequate subject numbers to determine whether an effect exists. Future studies should be of adequate duration (at least 6 years), recruit subjects from the seventh decade, choose markers of vitamin B12 status with adequate specificity such as holoTC and/or methylmalonic acid and employ standardised neurocognitive assessment tools and not screening tests in order to ascertain any relationship between vitamin B12 status and cognitive decline.

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.

Increased plasma homocysteine levels without signs of vitamin B12 deficiency in patients with multiple sclerosis assessed by blood and cerebrospinal fluid homocysteine and methylmalonic acid

2003 ◽  
Vol 9 (3) ◽  
pp. 239-245 ◽  
Author(s):  
M Vrethem ◽  
E Mattsson ◽  
H Hebelka ◽  
K Leerbeck ◽  
A Österberg ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Cerebrospinal Fluid ◽  
Methylmalonic Acid ◽  
Haemoglobin Concentration ◽  
Serum Vitamin ◽  
High Serum ◽  
Plasma Homocysteine ◽  
Cobalamin Deficiency ◽  
Vitamin B ◽  
Plasma Thcy

Objective: The aim of this study was to evaluate if multiple sclerosis (MS) is associated with vitamin B12 (cobalamin) deficiency. Methods: We measured serum vitamin B12, plasma folate, serum methylmalonic acid (MMA), plasma homocysteine (tHcy) and also cerebrospinal fluid (C SF) MMA and tHcy in 72 patients with MS and 23 controls. Results: The mean plasma tHcy level was significantly increased in MS patients (11.6 mmol/L) compared with controls (7.4 mmol/L) (P =4-0.002). Seven patients showed low serum vitamin B12levels but only one of them had concomitant high plasma tHcy. None of them showed high serum MMA. Plasma or blood folate levels did not differ between MS patients and controls. We found no significant differences in mean values or frequency of pathological tests of serum B12, serum MMA, mean corpuscular volume (MC V), haemoglobin concentration, C SF tHcy or C SF MMA between patients and healthy subjects. There were no correlations between C SF and serum/plasma levels of MMA or tHcy. Serum vitamin B12, serum MMA, plasma tHcy, C SF Hcy or C SF MMA were not correlated to disability status, activity of disease, duration of disease or age. Conclusions:The relevance of the increased mean value of plasma tHcy thus seems uncertain and does not indicate functional vitamin B12 deficiency. We can not, however, exclude the possibility of a genetically induced dysfunction of the homocysteine metabolism relevant for the development of neuroinflammation/degeneration. O ur findings indicate that, regardless of a significant increase in plasma tHcy in MS patients, the MS disease is not generally associated with vitamin B12 deficiency since we did not find any other factors indicating vitamin B12 deficiency. A nalysis of C SF MMA and C SF tHcy, which probably reflects the brain vitamin B12 status better than serum, are not warranted in MS. We conclude that B12 deficiency, in general, is not associated with MS.

scholarly journals Effects of cobalt deficiency in pregnant and post-parturient ewes and their lambs

1981 ◽  
Vol 46 (2) ◽  
pp. 337-344 ◽  
Author(s):  
W. R. H. Duncan ◽  
E. Rona Morrison ◽  
G. A. Garton
Keyword(s):  
Perinatal Mortality ◽  
Methylmalonic Acid ◽  
Post Partum ◽  
Acid Synthesis ◽  
Urinary Concentration ◽  
Vitamin B ◽  
Deficient Diet ◽  
Cobalt Deficiency ◽  
Group A ◽  
Group B

1. Two groups of ewes were fed on a cobalt-deficient diet throughout pregnancy; one group (group A) was given the diet from the beginning of pregnancy, whilst the other (group B) received the diet for 16 weeks before mating. The ewes in group A continued to receive the diet for 12 weeks post-partum.2. The vitamin B12 content of serum was estimated on three occasions before parturition and, for group A ewes, at 12 weeks post partum. Urinary concentration of methylmalonic acid was also determined at intervals before the lambs were born.3. Serum values for vitamin B12 indicated that the ewes in both groups were depleted of the vitamin, though those in group B were more severely affected, as was evidenced by the high incidence of perinatal mortality among the lambs born to these ewes. Perinatal mortality appeared to be associated with abnormally-high values for urinary concentration of methylmalonic acid.4. Analysis of liver lipids and adipose tissue triacylglycerols of some of the vitamin B12-deprived lambs which died before, or within 1 d of, birth showed that, compared with the corresponding tissues of control lambs, these lipids contained unusually high proportions of odd-numbered fatty acids (mostly 15:0, 17:0 and 19:0). This observation is discussed in relation to the likelihood that, in vitmain B12-deprived lambs, propionate becomes available as a primer unit for fatty acid synthesis when the metabolism of its carboxylation product, methylmalonic acid, is impaired due to partlal lack of a vitamin B12-containing enzyme system.

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.

Ischemic strokes secondary to vitamin B12 deficiency-induced hyperhomocystinemia

Neurology ◽  
1998 ◽  
Vol 51 (2) ◽  
pp. 622-624 ◽  
Author(s):  
LaRoy P. Penix
Keyword(s):  
Mean Corpuscular Volume ◽  
Serum Vitamin ◽  
Vitamin B12 Deficiency ◽  
Vitamin B ◽  
Loading Test ◽  
Schilling Test ◽  
B12 Deficiency ◽  
Recurrent Strokes ◽  
Methionine Loading Test

A 45-year-old woman sustained two ischemic cerebral infarctions 16 years after ileal resection for Crohn's disease. Her evaluation showed an elevated random serum homocystine level, a low serum vitamin B12 level, and an increased mean corpuscular volume (MCV) without anemia. A methionine-loading test resulted in a marked increase in the homocystine levels 2, 4, and 6 hours after the load. A Schilling test demonstrated a malabsorption of vitamin B12. Vitamin B12 injections normalized her fasting homocystine level and her MCV. She has had no recurrent strokes during a year follow-up.

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