scholarly journals Folic acid metabolism in vitamin B12-deficient sheep. Depletion of liver folates

1973 ◽  
Vol 136 (2) ◽  
pp. 279-293 ◽  
Author(s):  
Richard M. Smith ◽  
William S. Osborne-White
Keyword(s):  
Urinary Excretion ◽  
Vitamin B12 ◽  
Acid Metabolism ◽  
Vitamin B12 Deficiency ◽  
Deficient Diet ◽  
Severe Vitamin ◽  
Quantitative Estimates ◽  
Folic Acid Metabolism ◽  
B12 Deficiency ◽  
Microbiological Assays

1. Metabolism of folate was studied in six ewes in an advanced state of vitamin B12 deficiency as judged by voluntary food intake and in their pair-fed controls receiving vitamin B12. A group of four animals that were maintained throughout the experiment at pasture was also studied. 2. After 34–40 weeks on the cobalt-deficient diet urinary excretion of formiminoglutamate by four deficient animals was about 3.2mmol/day and this was not significantly decreased by injection of three of them with about 4.5μg of [2-14C]folate/kg body weight per day for 5 days. Three days after the last injection retention of [2-14C]folate by the livers of the deficient animals (5.5% of the dose) was lower than that of their pair-fed controls (26% of the dose) but there was no evidence of net retention of injected folate in the livers of either group. Urinary excretion of 14C indicated that renal clearance of folate may have been impaired in very severe vitamin B12 deficiency. 3. As estimated by microbiological assays total folates in the livers of animals at pasture (12.9μg/g) included about 24% of 5-methyltetrahydrofolate as compared with about 72% of a total of 12.5μg/g in three further ewes fed on a stock diet of wheaten hay-chaff and lucerne-chaff. Liver folates of vitamin B12-deficient animals (0.5μg/g) included about 88% of 5-methyltetrahydrofolate as compared with about 51% of a total of 5.2μg/g in pair-fed animals treated with vitamin B12. 4. Chromatography of liver folates of the pair-fed animals permitted quantitative estimates of the pteroylglutamates present. The results showed that the vitamin B12-deficient livers were more severely depleted of tetrahydrofolates and formyltetrahydrofolates than of methyltetrahydrofolates and that as the deficiency developed they were more severely depleted of the higher polyglutamates than of the monoglutamate within each of these classes. Results from animals injected with [2-14C]folate indicated an impairment of the exchange between pteroylmonoglutamates and pteroylpolyglutamates in the livers of deficient animals. 5. In vitamin B12-deficient animals with food intakes below 200g/day some of the liver folates were not completely reduced and some degradation of pteroylpolyglutamates was detected. The latter condition may have been associated with fatty liver. 6. The results are discussed in relation to current theories of vitamin B12–folate interactions.

scholarly journals Severe Vitamin B12 Deficiency in Pregnancy Mimicking HELLP Syndrome

2019 ◽  
Vol 2019 ◽  
pp. 1-4
Author(s):  
Shravya Govindappagari ◽  
Michelle Nguyen ◽  
Megha Gupta ◽  
Ramy M. Hanna ◽  
Richard M. Burwick
Keyword(s):  
Vitamin B12 ◽  
Pernicious Anemia ◽  
Thrombotic Microangiopathy ◽  
Hellp Syndrome ◽  
Atypical Hemolytic Uremic Syndrome ◽  
Vitamin B12 Deficiency ◽  
Severe Vitamin ◽  
Elevated Liver Enzymes ◽  
B12 Deficiency ◽  
In Pregnancy

Severe vitamin B12 deficiency may present with hematologic abnormalities that mimic thrombotic microangiopathy disorders such as hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome. We report a patient diagnosed with severe vitamin B12 deficiency, following termination of pregnancy for suspected preeclampsia and HELLP syndrome at 21 weeks’ gestation. When hemolysis and thrombocytopenia persisted after delivery, testing was performed to rule out other etiologies of thrombotic microangiopathy, including atypical hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, and vitamin B12 deficiency. This work-up revealed undetectable vitamin B12 levels and presence of intrinsic factor antibodies, consistent with pernicious anemia. Parenteral B12 supplementation was initiated, with subsequent improvement in hematologic parameters. Our case emphasizes the importance of screening for B12 deficiency in pregnancy, especially in at-risk women with unexplained anemia or thrombocytopenia. Moreover, providers should consider B12 deficiency and pernicious anemia in the differential diagnosis of pregnancy-associated thrombotic microangiopathy.

scholarly journals Factors affecting formiminoglutamic acid excretion in vitamin B12 deficiency

1970 ◽  
Vol 116 (4) ◽  
pp. 681-688 ◽  
Author(s):  
Hedley R. Marston ◽  
Shirley H. Allen
Keyword(s):  
Urinary Excretion ◽  
Vitamin B12 ◽  
Vitamin B12 Deficiency ◽  
Acid Excretion ◽  
Factors Affecting ◽  
Methyl Donors ◽  
Pteroylglutamic Acid ◽  
B12 Deficiency ◽  
Acid Status

1. Formiminoglutamic acid, a product of the catabolism of histidine, is excreted in abnormally large amounts in the urines of vitamin B12-deficient rats and of vitamin B12-deficient sheep; the excretion is reduced to negligible amounts after administration of vitamin B12. 2. After administration of certain methyl donors to vitamin B12-deficient rats or sheep urinary excretion of formiminoglutamic acid is temporarily decreased. 3. Irrespective of the pteroylglutamic acid status of the animals neither vitamin B12-deficient rats nor vitamin B12-deficient sheep have the ability to deal efficiently with histidine. 4. In sheep, urinary excretion of formiminoglutamic acid is increased after administration of aminopterin; treatment with pteroylglutamic acid restores the ability of the animal to deal with the catabolic products of histidine. 5. The possible functions of vitamin B12 and methionine in relieving a virtual deficiency of pteroylglutamic acid are discussed.

scholarly journals A Dietary Vitamin B12 Deficiency Impairs Balance and Coordination After Ischemic Injury to the Sensorimotor Cortex in Adult Male and Female Mice

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 932-932
Author(s):  
Gyllian Yahn ◽  
Brandi Wasek ◽  
Terry Bottiglieri ◽  
Nafisa Jadavji
Keyword(s):  
Risk Factor ◽  
Ischemic Stroke ◽  
Vitamin B12 ◽  
Vitamin B12 Deficiency ◽  
Stroke Outcome ◽  
Deficient Diet ◽  
Male And Female ◽  
Female Mice ◽  
B12 Deficiency ◽  
Total Homocysteine

Abstract Objectives The majority of the world's population is growing older, in 2000, 10% of the total population of the world was over 60 years old and is projected to increase to 21% by 2050. Brain vasculature is unique, and its aging has been scarcely investigated at the cellular, and molecular levels, as well as in the context of age-related comorbidities. Nutrition is a modifiable risk factor for stroke, as people age their ability to absorb some nutrients decreases. A primary example is vitamin B12, the majority of older adults are deficient in vitamin B12 because of changes in breakdown and absorption of the vitamin. Furthermore, a vitamin B12 deficiency results in elevated levels of homocysteine which is a risk factor for cardiovascular diseases, such as stroke. Using a mouse model system, the aim of this study was to understand the role of vitamin B12 deficiency in ischemic stroke outcome and investigate mechanistic changes in the brain. Methods At 10-weeks of age male and female C57Bl/6J mice were put on control (0.025 mg/kg of vitamin B12) or vitamin B12 deficient (0 mg/kg of vitamin B12) diets for 4-weeks prior to ischemic damage. At 14 weeks of age we induced ischemic stroke in the sensorimotor cortex using the photothrombosis model, all animals received damage. Animals continued on diets for 4 weeks after damage. At 18 weeks of age we assessed stroke outcome using the accelerating rotarod and forepaw placement task. After the collection of behavioral data, we euthanized animals and collected brain, blood, and liver tissue to assess histological and biochemical measurements. Plasma was used to measure total homocysteine and methylmalonic acid. Results All animals maintained on the vitamin B12 deficient diet had increased levels of total homocysteine in plasma and liver tissue. Male and female mice maintained on a vitamin B12 deficient diet had impairments in balance and coordination on the accelerating rotarod compared to animals maintained on a control diet. Conclusions Vitamin B12 deficiency impacts motor function in older adult male and female mice. We are investigating damage volume and potential mechanisms within the damage brain tissue. Funding Sources Midwestern University Start-Up Funds.

scholarly journals Life-threatening Pseudo-thrombotic Microangiopathy Caused by Severe Vitamin B12 Deficiency

2021 ◽  
Vol 9 (11) ◽  
pp. 532-534
Author(s):  
Ziad Abuhelwa ◽  
Talal Khan ◽  
Rana Daas ◽  
Sami Ghazaleh ◽  
Ragheb Assaly
Keyword(s):  
Vitamin B12 ◽  
Thrombotic Microangiopathy ◽  
Vitamin B12 Deficiency ◽  
Severe Vitamin ◽  
Life Threatening ◽  
B12 Deficiency
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