Vitamin B12 is a collection of cobalt and corrin ring molecules working as cofactors in specific enzymatic reactions and whose synthesis take place in bacteria.
Vitamin B12
Role
Commercial Presentation of Vitamin B12
Intestinal Vitamin B12 uptake
Vitamin B12, folic acid, and the nervous system. 2006
Reactions involving Vit B12
>. Serena Masellis 12/01/2014
VITAMIN B 12
Vitamin B 12 or Cobalamin
is present in very little quantity in aliments of animal origin; the most rich organs are heart, liver and kidneys. The total absentia of Cobalamin in vegetal foods is the reason why the most part of the B 12 Hypovitaminosis hurts especially vegan people (who don’t eat neither cheese, nor eggs and milk).
Battery flora can synthesize vitamin B 12, but in such a low quantity that this is not enough to provide for human daily requirement (only 2-3 micrograms/die).
Vitamin B 12 can be converted in the human body in different forms of the same vitamin:
- Hydroxicobilamin (R = –OH),
- Cyanocobalamin (R = –CN),
- Methylcobalamin (R = –CH3) an active form of the vitamin,
- Adenosyilcobalamin (R = –Ado) another active form of the vitamin.
The absorption of Vitamin b12 in the human organism is mediated by some proteins that create a chemical bond with this molecule from its entry in the mouth until its absorption in the intestine.
AMNLS_HUMAN
Inherited cobalamin malabsorption. Mutations in three genes reveal functional and ethnic patterns,2012
TCO1_HUMAN
Transcobalamin-1
TCN1 T Haptocorrin?
IF_HUMAN
Gastric intrinsic factor
GIF
The deficiency of Vitamin B12 is caused by:
- Deficiency in the alimentation of Vitamin B˜12
- Deficiency of the Intrinsecal Factor (also named Castle Factor secreted by parietal cells of the stomach)
- Bacterial or parassitarial interference in the normal absorption of vitamin b12 along the digestive system
- Reduced capacity of the intestinal wall in the absorption of the vitamin.
This deficiency causes anemic state and some neurologic problems including rapid changing of humor and "Major Depressive Disorder" :http://en.wikipedia.org/wiki/Major_depressive_disorder together with other neurological disorders.
Another important molecule in this insurgence is Folic Acid (E. Reynolds—Vitamin B12, folic acid, and the nervous system).
See also Vitamin B12 and depression
aggiunta di Serena Mase
The soluble transcobalamin receptor (sCD320) is present in cerebrospinal fluid and correlates to dementia-related biomarkers tau proteins and amyloid-beta. 2015
BACKGROUND:
Cellular uptake of vitamin B12 (B12) demands binding of the vitamin to transcobalamin (TC) and recognition of TC-B12 (holoTC) by the receptor CD320. Recently, we identified a soluble form of CD320 (sCD320) in human plasma. Here we present data on the occurrence of this soluble receptor in cerebrospinal fluid (CSF) and show its correlations to dementia-related biomarkers tau proteins and amyloid-beta.
METHODS:
We collected 223 cerebrospinal fluid samples and corresponding plasma samples (n = 46). We measured CSF and plasma sCD320, holoTC and total TC employing in-house ELISA methods and CSF phospho-tau (181P) (p-tau), total tau (t-tau) and amyloid-beta 1-42 (Aβ) (n = 177) employing commercial ELISA kits (Innogenetics Company). Size exclusion chromatography was performed on a Superdex 200 column.
RESULTS:
The median sCD320 concentration in CSF (14 pmol/L) is around five times lower than in plasma (72 pmol/L). No correlation was observed between plasma and CSF sCD320 levels (n = 46), while the behavior upon size exclusion chromatography was the same. In CSF, sCD320 correlates to holoTC and total TC (Spearman's correlation (Rs) = 0.325, 0.232 (n = 218, 217) respectively, p < 0.01). Interestingly, sCD320 correlates to p-tau and t-tau (Rs = 0.599, 0.569 (n = 173, 176) respectively, p < 0.001) and to Aβ (Rs = 0.265, p < 0.001 (n = 177)).
CONCLUSION:
We document for the first time the occurrence of sCD320 in human CSF. We report that the concentration of sCD320 correlates to the dementia-related biomarkers p-tau, t-tau and Aβ.
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Transcobalamin derived from bovine milk stimulates apical uptake of vitamin B12 into human intestinal epithelial cells. 2012
Abstract
Intestinal uptake of vitamin B12 (hereafter B12) is impaired in a significant proportion of the human population. This impairment is due to inherited or acquired defects in the expression or function of proteins involved in the binding of diet-derived B12 and its uptake into intestinal cells. Bovine milk is an abundant source of bioavailable B12 wherein it is complexed with transcobalamin. In humans, transcobalamin functions primarily as a circulatory protein, which binds B12 following its absorption and delivers it to peripheral tissues via its cognate receptor, CD320. In the current study, the transcobalamin-B12 complex was purified from cows' milk and its ability to stimulate uptake of B12 into cultured bovine, mouse and human cell lines was assessed. Bovine milk-derived transcobalamin-B12 complex was absorbed by all cell types tested, suggesting that the uptake mechanism is conserved across species. Furthermore, the complex stimulated the uptake of B12 via the apical surface of differentiated Caco-2 human intestinal epithelial cells. These findings suggest the presence of an alternative transcobalamin-mediated uptake pathway for B12 in the human intestine other than that mediated by the gastric glycoprotein, intrinsic factor. Our findings highlight the potential for transcobalamin-B12 complex derived from bovine milk to be used as a natural bioavailable alternative to orally administered free B12 to overcome B12 malabsorption.
Influence of duration and dose of metformin on cobalamin deficiency in type 2 diabetes patients using metformin. 2015
Metformin use is associated with cobalamin (vitamin B12) deficiency. However, the influence of both duration and dose of metformin is unclear. Studies using holotranscobalamin, a marker for cellular cobalamin deficiency, are scarce. We therefore investigated the prevalence of cobalamin deficiency in type 2 diabetes patients using both markers, and its relation with duration and dose of metformin use. This cross-sectional study among 550 type 2 diabetes patients using metformin (mean daily dose 1,306 mg; mean duration 64 months) was conducted in four primary care centers in Utrecht, the Netherlands. Cobalamin and holotranscobalamin concentrations were measured at the annual diabetes check. Detailed information on metformin use and confounding variables was collected from medical records. The prevalence of a cobalamin deficiency was 28.1 , while a holotranscobalamin deficiency occurred in 3.9 of the patients. Adjusting for multiple confounders, a 1 mg/day increase in daily metformin dose was associated (p < 0.001) with 0.042 (95 % CI -0.060, -0.023) decrease in cobalamin concentrations. Similarly, a 10 g increase of cumulative metformin dose was associated (p = 0.006) with -0.070 (-0.12, -0.021) lower cobalamin concentrations after adjustment for confounders. Duration of metformin use was not associated with cobalamin concentrations after multivariable adjustment. Similar results were observed for holotranscobalamin. Cobalamin deficiency occurs frequently among diabetes patients using metformin. A higher daily and cumulative doses of metformin were strongly associated with lower cobalamin and holotranscobalamin concentrations, while duration was not. It is thus important to account for metformin dose in recommendations for screening for cobalamin deficiency.
haptocorrin+gene utile per Alzheimer
Genomic structure and mapping of the chromosomal gene for transcobalamin I (TCN1): comparison to human intrinsic factor. 1992
Abstract
Transcobalamin I (TCI) is a vitamin B12 binding protein that is found in the secondary granules of mature neutrophils. The expression of the gene for TCI (TCN1) within neutrophils has been shown to be restricted to the later stages of myeloid development and can therefore be used as a marker for granulocyte differentiation. To study transcriptional control regions important in late stage myeloid gene regulation the genomic sequence for TCN1 has been cloned. Clones were isolated from a genomic library constructed in Charon 4A using homologous full-length cDNA probes. Southern blot analysis showed the gene to reside on five EcoRI fragments totaling 14 kb in length. Two overlapping phage clones, containing the entire 14 kb, were isolated and the introns and exons were mapped using Southern blotting and dideoxy sequencing of subclones. The cDNA is represented by nine exons contained within 12 kb of genomic DNA. Comparison of the genomic structure to gastric intrinsic factor (GIF), another vitamin B12 binding protein, revealed a strikingly similar intron/exon structure, with several positionally conserved splice sites. The gene was localized to chromosome 11 using in situ hybridization.
TCN1 Transcobalamin I (Vitamin B12 Binding Protein, R Binder Family) Protein Coding 53 GC11M059871 22.11
2 TCN2 Transcobalamin II Protein Coding 57 GC22P030606 6.24
3 GIF Gastric Intrinsic Factor (Vitamin B Synthesis) Protein Coding 59 GC11M059847 4.94
4 EGF Epidermal Growth Factor Protein Coding 69 GC04P109912 3.12
5 CBL Cbl Proto-Oncogene, E3 Ubiquitin Protein Ligase Protein Coding 66 GC11P119206 2.21
6 CUBN Cubilin (Intrinsic Factor-Cob
