The Quantitative Determination of Vitamin B12 Concentration in Human Serum by a Microplate Chemiluminescence Immunoassay.
Storage
2-8°C
Sensitivity
70.13 pg/ml
General Description
Vitamin B12 (cobalamin) is one of the 13 vitamins essential to human health and life. It is crucial for the construction of DNA, production of red blood cells and aids in the maintenance of a healthy nervous system. B12 deficiency damages the brain, spinal cord, peripheral nerves, and nerves of the eye. A B12 deficiency can result in symptoms ranging from severe anemia requiring blood transfusions, fatigue, muscle soreness, memory loss, and behavioral changes to serious and permanent nerve damage. B12 is found naturally in animal foods or is received through supplements, and must follow a complex pathway of several steps for proper absorption. CD's assay measures total B12 in serum.
Citations
Publication ()
Have you cited DEIACL6 in a publication? Let us know and earn a reward for your research.
Background
Closely related to folic acid, vitamin B12 (B12), also known as cobalamin, plays an important role in cellular metabolism. With the discovery of the close relationship between B12 and pernicious anemia, people have learned more about B12 deficiency. Previously thought to be a nutritional deficiency mainly caused by vitamin malabsorption, B12 deficiency is now considered to be a global problem often caused by dietary deficiencies, especially among children and women of childbearing age. The earliest classic clinical manifestation of B12 deficiency was pernicious anemia, and as research progressed, it became clear that B12 deficiency primarily caused hematologic and neurologic disorders. In the absence of hematologic disorders, B12 deficiency can also affect the nervous system, causing ataxia, sensory and motor deficits, and cognitive decline leading to dementia. Between normal B12 levels and clinical deficiency there is a phase of insufficient B12 levels, during which biochemical evidence manifests itself in the form of elevated blood and tissue levels of MMA and homocysteine, as well as decreased levels of the portion of B12 that binds to transcobalamin, before any morbid manifestations of deficiency occur. This condition is also known as "subclinical" B12 deficiency.
Figure 1. B12 and folate metabolism and function (Source: Green R, et al. 2017)
The most commonly used marker in laboratory testing is the total abundance of B12 in serum, and the threshold for clinical diagnosis of B12 deficiency is usually set at 148 pmol/L (200 ng/L). Automated assays for holotranscobalamin (known as "active B12"), which is a form of B12 that is taken up by cells to meet their metabolic needs, have since emerged, providing an alternative method for assessing B12 status. Sensitive functional indicators of B12 status, such as the measurement of total homocysteine (tHcy) and methylmalonic acid (MMA) in serum, have also been automated.
Our product [DEIACL6] adopts the principle of chemiluminescence to detect the total abundance of human serum B12, and the sensitivity can reach 70.13 pg/mL. The product adopts delayed competitive enzyme immunoassay. After the biotinylated antibody is mixed with the serum containing antigen, the antigen and antibody will react. After a short incubation, the enzyme conjugate was added, and the enzyme analogue and the antigen in the sample competed on a limited number of antibody binding sites (which were not consumed at the first incubation). The enzyme activity of antibody binding part is inversely proportional to the concentration of primary antigen. By using several different serum references with known antigen concentrations, a dose response curve can be generated to determine the concentration of unknown antigens.
My Review for CDSimple™ Vitamin B12 Chemiluminescent ELISA Kit
Creative Diagnostics products are for RESEARCH USE ONLY, please make sure your review is research based.
Required fields are marked with *
Terms and conditions:
We will select high-quality review customers and offer a $30 coupon for your next purchase.
All product reviews must be submitted in the English language.
Creative Diagnostics will not share any personal information of applicants, and all information will be treated with strict confidentiality and will not be sold or disclosed to a third party.
References
Effects of Vitamin B12 Supplementation on Cognitive Function, Depressive Symptoms, and Fatigue: A Systematic Review, Meta-Analysis, and Meta-Regression
Nutrients
Authors: Markun S, Gravestock I, Jäger L, Rosemann T, Pichierri G, Burgstaller JM.
Vitamin B12 is often used to improve cognitive function, depressive symptoms, and fatigue. In most cases, such complaints are not associated with overt vitamin B12 deficiency or advanced neurological disorders and the effectiveness of vitamin B12 supplementation in such cases is uncertain. The aim of this systematic review and meta-analysis of randomized controlled trials (RCTs) is to assess the effects of vitamin B12 alone (B12 alone), in addition to vitamin B12 and folic acid with or without vitamin B6 (B complex) on cognitive function, depressive symptoms, and idiopathic fatigue in patients without advanced neurological disorders or overt vitamin B12 deficiency. Medline, Embase, PsycInfo, Cochrane Library, and Scopus were searched. A total of 16 RCTs with 6276 participants were included. Regarding cognitive function outcomes, we found no evidence for an effect of B12 alone or B complex supplementation on any subdomain of cognitive function outcomes. Further, meta-regression showed no significant associations of treatment effects with any of the potential predictors. We also found no overall effect of vitamin supplementation on measures of depression. Further, only one study reported effects on idiopathic fatigue, and therefore, no analysis was possible. Vitamin B12 supplementation is likely ineffective for improving cognitive function and depressive symptoms in patients without advanced neurological disorders
Vitamin B12 is assimilated and transported by complex mechanisms that involve three transport proteins, intrinsic factor (IF), haptocorrin (HC) and transcobalamin (TC) and their respective membrane receptors. Vitamin deficiency is mainly due to inadequate dietary intake in vegans, and B12 malabsorption is related to digestive diseases. This review explores the physiology of vitamin B12 absorption and the mechanisms and diseases that produce malabsorption. In the stomach, B12 is released from food carrier proteins and binds to HC. The degradation of HC by pancreatic proteases and the pH change trigger the transfer of B12 to IF in the duodenum. Cubilin and amnionless are the two components of the receptor that mediates the uptake of B12 in the distal ileum. Part of liver B12 is excreted in bile, and undergoes an enterohepatic circulation. The main causes of B12 malabsorption include inherited disorders (Intrinsic factor deficiency, Imerslund-Gr?sbeck disease, Addison's pernicious anemia, obesity, bariatric surgery and gastrectomies. Other causes include pancreatic insufficiency, obstructive Jaundice, tropical sprue and celiac disease, bacterial overgrowth, parasitic infestations, Zollinger-Ellison syndrome, inflammatory bowel diseases, chronic radiation enteritis of the distal ileum and short bowel. The assessment of B12 deficit is recommended in the follow-up of subjects with bariatric surgery. The genetic causes of B12 malabsorption are probably underestimated in adult cases with B12 deficit. Despite its high prevalence in the general population and in the elderly, B12 malabsorption cannot be anymore assessed by the Schilling test, pointing out the urgent need for an equivalent reliable test.
COA
Publication 
Figure 1. B12 and folate metabolism and function
Loading ......
