MC-04 The effects of a 2x Vitamin B12 treatment on expression of epigenetic modifying proteins in a human neuronal cell model

Start Date

31-3-2023 10:30 AM

End Date

31-3-2023 12:30 PM

Document Type

Poster

Abstract

Vitamin B12 is one of the most commonly found vitamins in foods, drinks, and supplements. Most research has only focused on vitamin B12 deficiency. Studies indicated that roughly 14.5% of outpatient elderly patients have these deficiencies. Patients are treated with high levels of Vitamin B12 through injections and oral supplements.

Recently, serum Vitamin B12 levels at twice the average “normal” Vitamin B12 levels have been documented, which is known as hypercobalaminemia, which affects an individual in their gastrointestinal and nervous systems. Vitamin B12 aids in metabolism of folic acid in the one carbon metabolic pathway that adds methyl groups to DNA and histones. These methyl groups on DNA and histone modifications like methylation and acetylation change gene expression without altering gene sequence in what is known as epigenetics. Epigenetic marks are altered as part of the aging process, and this results in changed genes’ expression with aging.

We used three different forms of vitamin B12: +2 Cobalt, +3 Cobalt, and cobamamide. To see how excess vitamin B12 levels affect human neuronal SH-SY5Y cells, each form was given in twice the normal amount to mimic the 2x serum levels noted in clinical settings. The cells used in this study were given less nutritious cell food so that they would take up more of the vitamin B12. We studied the gene expressions of the following targets: DNA methyltransferase 3A (DNMT3A), DNA methyltransferase 1 (DNMT1), and methyl-CpG binding protein 2 (MECP2).

We hypothesized that there are various changes in these genes’ expression levels which might affect epigenetics, and we expected to see decreases in DNMT3A, DNMT1, and MECP2 since DNA methylation traditionally decreases in aging individuals. Upon completion of this project, we hope to have a better understanding of the effects of Vitamin B12 overconsumption on neurons.

This document is currently not available here.

Share

COinS
 
Mar 31st, 10:30 AM Mar 31st, 12:30 PM

MC-04 The effects of a 2x Vitamin B12 treatment on expression of epigenetic modifying proteins in a human neuronal cell model

Vitamin B12 is one of the most commonly found vitamins in foods, drinks, and supplements. Most research has only focused on vitamin B12 deficiency. Studies indicated that roughly 14.5% of outpatient elderly patients have these deficiencies. Patients are treated with high levels of Vitamin B12 through injections and oral supplements.

Recently, serum Vitamin B12 levels at twice the average “normal” Vitamin B12 levels have been documented, which is known as hypercobalaminemia, which affects an individual in their gastrointestinal and nervous systems. Vitamin B12 aids in metabolism of folic acid in the one carbon metabolic pathway that adds methyl groups to DNA and histones. These methyl groups on DNA and histone modifications like methylation and acetylation change gene expression without altering gene sequence in what is known as epigenetics. Epigenetic marks are altered as part of the aging process, and this results in changed genes’ expression with aging.

We used three different forms of vitamin B12: +2 Cobalt, +3 Cobalt, and cobamamide. To see how excess vitamin B12 levels affect human neuronal SH-SY5Y cells, each form was given in twice the normal amount to mimic the 2x serum levels noted in clinical settings. The cells used in this study were given less nutritious cell food so that they would take up more of the vitamin B12. We studied the gene expressions of the following targets: DNA methyltransferase 3A (DNMT3A), DNA methyltransferase 1 (DNMT1), and methyl-CpG binding protein 2 (MECP2).

We hypothesized that there are various changes in these genes’ expression levels which might affect epigenetics, and we expected to see decreases in DNMT3A, DNMT1, and MECP2 since DNA methylation traditionally decreases in aging individuals. Upon completion of this project, we hope to have a better understanding of the effects of Vitamin B12 overconsumption on neurons.