Reviewed By
Overview
SCIENTIFIC SCORE
Possibly Effective
Based on 22 Researches
7.3
USERS' SCORE
Good
Based on 3 Reviews
8.4
Supplement Facts
Serving Size: 1 Tablet
Amount Per Serving
%DV
Vitamin B₆ (as Pyridoxal 5-Phosphate)
2.5 mg
147%
Folate (800 mcg as 6S)-5MTHF-Methyltetrahydrofolate Glucosamine Salt)
1,360 mcg DFE‡
340%
Vitamin B12 (as Methylcobalamin)
5,000 mcg
208,330%
Top Medical Research Studies
9
Folate treatment aids liver fat reduction
We investigated the effects of folic acid treatment on nonalcoholic fatty liver disease (NAFLD), a condition where excess fat builds up in the liver, often linked to obesity and insulin resistance. Our research revealed that giving folic acid to mice on a high-fat diet helped improve their glucose tolerance and insulin sensitivity, alongside reducing unhealthy fat levels in their liver cells.
By diving into the mechanisms, we discovered that folic acid works by changing the DNA methylation patterns that regulate the expression of a protein called ALKBH5. This reduction in ALKBH5 levels led to an increase in a specific type of RNA modification and subsequently boosted the production of a protein called ATG12, which is vital for autophagy – the process that cleans up and recycles cellular components.
When we inhibited ATG12 through overexpression of ALKBH5, autophagy was impeded, showcasing how crucial ATG12 is for allowing folic acid to effectively reduce fat accumulation in the liver. Overall, these findings indicate that folic acid could be a promising nutritional ally in fighting NAFLD, revealing a clear mechanism by which it protects liver health.
By diving into the mechanisms, we discovered that folic acid works by changing the DNA methylation patterns that regulate the expression of a protein called ALKBH5. This reduction in ALKBH5 levels led to an increase in a specific type of RNA modification and subsequently boosted the production of a protein called ATG12, which is vital for autophagy – the process that cleans up and recycles cellular components.
When we inhibited ATG12 through overexpression of ALKBH5, autophagy was impeded, showcasing how crucial ATG12 is for allowing folic acid to effectively reduce fat accumulation in the liver. Overall, these findings indicate that folic acid could be a promising nutritional ally in fighting NAFLD, revealing a clear mechanism by which it protects liver health.
Read More
9
We explored how methylcobalamin, a form of vitamin B12, impacts liver disease, particularly in the context of cholestatic liver failure. The study utilized high-throughput screening to identify methylcobalamin as a specific inhibitor of gasdermin E (GSDME), a protein that plays a key role in pyroptotic cell death—a form of inflammatory cell death contributing to liver damage.
Our findings showed that when tested on mouse models with liver failure due to cholestasis, cisplatin, or concanavalin A, methylcobalamin effectively reduced liver damage. It significantly lowered liver transaminase levels, indicating less liver inflammation and cellular injury, and helped alleviate overall liver cell death.
Furthermore, methylcobalamin worked by preventing the cleavage of GSDME, which is essential for uncontrolled inflammatory cell death. By binding to a specific site on the GSDME protein, it blocked the interactions that trigger this damaging process. Overall, our study highlighted the potential of methylcobalamin as a promising therapeutic option for managing cholestatic liver failure and related conditions.
Our findings showed that when tested on mouse models with liver failure due to cholestasis, cisplatin, or concanavalin A, methylcobalamin effectively reduced liver damage. It significantly lowered liver transaminase levels, indicating less liver inflammation and cellular injury, and helped alleviate overall liver cell death.
Furthermore, methylcobalamin worked by preventing the cleavage of GSDME, which is essential for uncontrolled inflammatory cell death. By binding to a specific site on the GSDME protein, it blocked the interactions that trigger this damaging process. Overall, our study highlighted the potential of methylcobalamin as a promising therapeutic option for managing cholestatic liver failure and related conditions.
Read More
9
Methylcobalamin improves nerve myelination
We delved into the effects of methylcobalamin, a form of vitamin B12, on nerve myelination in rats suffering from moderate hepatic encephalopathy, a condition caused by ammonia toxicity due to liver dysfunction. In our study, we established a model of hepatic encephalopathy by administering thioacetamide to induce liver damage, subsequently leading to changes in nerve myelination in specific brain regions.
We focused on the hippocampus, an area crucial for memory and learning, where we noted significant reductions in myelin levels and myelin basic protein (MBP) quantities in the affected rats. However, after administering methylcobalamin for a week, we observed a remarkable recovery in the myelination status, alongside normalized levels of harmful homocysteine, which is regulated by the enzyme methionine synthase that methylcobalamin helps activate.
Our findings suggest that methylcobalamin effectively restores nerve myelination in the context of liver disease by addressing underlying biochemical changes. The treatment not only improved myelination but also showed promise in restoring neurobehavioral functions in the rats. This research indicates a potential therapeutic role for vitamin B12 in managing liver-related nerve damage, making it worth further exploration in human studies.
We focused on the hippocampus, an area crucial for memory and learning, where we noted significant reductions in myelin levels and myelin basic protein (MBP) quantities in the affected rats. However, after administering methylcobalamin for a week, we observed a remarkable recovery in the myelination status, alongside normalized levels of harmful homocysteine, which is regulated by the enzyme methionine synthase that methylcobalamin helps activate.
Our findings suggest that methylcobalamin effectively restores nerve myelination in the context of liver disease by addressing underlying biochemical changes. The treatment not only improved myelination but also showed promise in restoring neurobehavioral functions in the rats. This research indicates a potential therapeutic role for vitamin B12 in managing liver-related nerve damage, making it worth further exploration in human studies.
Read More
Most Useful Reviews
7.5
Improved calmness
This was recommended by my nutritionist, and since then, my sleep has improved and I've felt calmer. I’m keen to undertake another course to continue addressing my liver disease.
Read More
9
Lowers homocysteine levels
2 people found this helpful
I use this to reduce my homocysteine levels, which are linked to heart disease, including liver disease. It is essential to have the methylated versions of these vitamins.
Read More
7.5
Good for assimilation
3 people found this helpful
I purchased this remedy for my elderly father, who suffers from blood clots and liver disease. It has a pleasant taste and did not cause any adverse reactions, despite his liver issues. The dosage is good, with the active folate form allowing for better absorption of the vitamin complex. I will order more.
Read More
Medical Researches
SCIENTIFIC SCORE
Possibly Effective
Based on 22 Researches
7.3
- All Researches
9
Folate treatment aids liver fat reduction
We investigated the effects of folic acid treatment on nonalcoholic fatty liver disease (NAFLD), a condition where excess fat builds up in the liver, often linked to obesity and insulin resistance. Our research revealed that giving folic acid to mice on a high-fat diet helped improve their glucose tolerance and insulin sensitivity, alongside reducing unhealthy fat levels in their liver cells.
By diving into the mechanisms, we discovered that folic acid works by changing the DNA methylation patterns that regulate the expression of a protein called ALKBH5. This reduction in ALKBH5 levels led to an increase in a specific type of RNA modification and subsequently boosted the production of a protein called ATG12, which is vital for autophagy – the process that cleans up and recycles cellular components.
When we inhibited ATG12 through overexpression of ALKBH5, autophagy was impeded, showcasing how crucial ATG12 is for allowing folic acid to effectively reduce fat accumulation in the liver. Overall, these findings indicate that folic acid could be a promising nutritional ally in fighting NAFLD, revealing a clear mechanism by which it protects liver health.
By diving into the mechanisms, we discovered that folic acid works by changing the DNA methylation patterns that regulate the expression of a protein called ALKBH5. This reduction in ALKBH5 levels led to an increase in a specific type of RNA modification and subsequently boosted the production of a protein called ATG12, which is vital for autophagy – the process that cleans up and recycles cellular components.
When we inhibited ATG12 through overexpression of ALKBH5, autophagy was impeded, showcasing how crucial ATG12 is for allowing folic acid to effectively reduce fat accumulation in the liver. Overall, these findings indicate that folic acid could be a promising nutritional ally in fighting NAFLD, revealing a clear mechanism by which it protects liver health.
Read More
9
We explored how methylcobalamin, a form of vitamin B12, impacts liver disease, particularly in the context of cholestatic liver failure. The study utilized high-throughput screening to identify methylcobalamin as a specific inhibitor of gasdermin E (GSDME), a protein that plays a key role in pyroptotic cell death—a form of inflammatory cell death contributing to liver damage.
Our findings showed that when tested on mouse models with liver failure due to cholestasis, cisplatin, or concanavalin A, methylcobalamin effectively reduced liver damage. It significantly lowered liver transaminase levels, indicating less liver inflammation and cellular injury, and helped alleviate overall liver cell death.
Furthermore, methylcobalamin worked by preventing the cleavage of GSDME, which is essential for uncontrolled inflammatory cell death. By binding to a specific site on the GSDME protein, it blocked the interactions that trigger this damaging process. Overall, our study highlighted the potential of methylcobalamin as a promising therapeutic option for managing cholestatic liver failure and related conditions.
Our findings showed that when tested on mouse models with liver failure due to cholestasis, cisplatin, or concanavalin A, methylcobalamin effectively reduced liver damage. It significantly lowered liver transaminase levels, indicating less liver inflammation and cellular injury, and helped alleviate overall liver cell death.
Furthermore, methylcobalamin worked by preventing the cleavage of GSDME, which is essential for uncontrolled inflammatory cell death. By binding to a specific site on the GSDME protein, it blocked the interactions that trigger this damaging process. Overall, our study highlighted the potential of methylcobalamin as a promising therapeutic option for managing cholestatic liver failure and related conditions.
Read More
9
Methylcobalamin improves nerve myelination
We delved into the effects of methylcobalamin, a form of vitamin B12, on nerve myelination in rats suffering from moderate hepatic encephalopathy, a condition caused by ammonia toxicity due to liver dysfunction. In our study, we established a model of hepatic encephalopathy by administering thioacetamide to induce liver damage, subsequently leading to changes in nerve myelination in specific brain regions.
We focused on the hippocampus, an area crucial for memory and learning, where we noted significant reductions in myelin levels and myelin basic protein (MBP) quantities in the affected rats. However, after administering methylcobalamin for a week, we observed a remarkable recovery in the myelination status, alongside normalized levels of harmful homocysteine, which is regulated by the enzyme methionine synthase that methylcobalamin helps activate.
Our findings suggest that methylcobalamin effectively restores nerve myelination in the context of liver disease by addressing underlying biochemical changes. The treatment not only improved myelination but also showed promise in restoring neurobehavioral functions in the rats. This research indicates a potential therapeutic role for vitamin B12 in managing liver-related nerve damage, making it worth further exploration in human studies.
We focused on the hippocampus, an area crucial for memory and learning, where we noted significant reductions in myelin levels and myelin basic protein (MBP) quantities in the affected rats. However, after administering methylcobalamin for a week, we observed a remarkable recovery in the myelination status, alongside normalized levels of harmful homocysteine, which is regulated by the enzyme methionine synthase that methylcobalamin helps activate.
Our findings suggest that methylcobalamin effectively restores nerve myelination in the context of liver disease by addressing underlying biochemical changes. The treatment not only improved myelination but also showed promise in restoring neurobehavioral functions in the rats. This research indicates a potential therapeutic role for vitamin B12 in managing liver-related nerve damage, making it worth further exploration in human studies.
Read More
9
We explored the intriguing question of whether vitamin B12 can provide a protective effect against liver damage caused by acetaminophen, a common painkiller known for its potential hepatotoxicity. In our study, we used male Wister rats and organized them into three groups: one receiving acetaminophen, another treated with vitamin B12, and a control group given distilled water. Each group was administered their respective treatments for a week before we evaluated their liver health.
Our findings indicate that vitamin B12 supplementation significantly improved hepatic health in the rats exposed to acetaminophen. We observed a notable reduction in liver enzyme levels, which is a key marker of liver damage. Additionally, vitamin B12 helped boost antioxidant levels in the body, compensated for a decline in tissue glutathione, and reduced harmful inflammatory markers such as TNF-α and interleukin-6.
Overall, the results of our study suggest that vitamin B12 effectively mitigates acetaminophen-induced liver toxicity by enhancing liver function and reducing inflammation. This insight opens up interesting avenues for considering vitamin B12 as a supportive treatment in managing liver health in cases of acetaminophen exposure.
Our findings indicate that vitamin B12 supplementation significantly improved hepatic health in the rats exposed to acetaminophen. We observed a notable reduction in liver enzyme levels, which is a key marker of liver damage. Additionally, vitamin B12 helped boost antioxidant levels in the body, compensated for a decline in tissue glutathione, and reduced harmful inflammatory markers such as TNF-α and interleukin-6.
Overall, the results of our study suggest that vitamin B12 effectively mitigates acetaminophen-induced liver toxicity by enhancing liver function and reducing inflammation. This insight opens up interesting avenues for considering vitamin B12 as a supportive treatment in managing liver health in cases of acetaminophen exposure.
Read More
8
We explored the effects of vitamin B6 in combating nonalcoholic fatty liver disease (NAFLD) through a study that utilized a mouse model. The mice were fed a diet designed to induce NAFLD, and then we treated them with green pea hull polyphenol extract, which is rich in beneficial compounds, including vitamin B6.
Our findings revealed that vitamin B6 plays a crucial role in alleviating the symptoms of NAFLD. We observed that after the intervention with the green pea extract, the vitamin B6 levels significantly increased in the mice's livers. This surge in vitamin B6 appears to activate important signaling pathways that aid in reducing fat accumulation in the liver, enhancing antioxidant activity, and improving overall lipid metabolism.
Moreover, we noted that increased intestinal permeability was linked to a worsening of NAFLD symptoms. With the help of cutting-edge metabolomics and transcriptomic analysis, we pinpointed the significance of vitamin B6, which may act as a metabolite produced by gut bacteria. This insight suggests a promising direction for NAFLD treatments that incorporate dietary sources of vitamin B6.
Our findings revealed that vitamin B6 plays a crucial role in alleviating the symptoms of NAFLD. We observed that after the intervention with the green pea extract, the vitamin B6 levels significantly increased in the mice's livers. This surge in vitamin B6 appears to activate important signaling pathways that aid in reducing fat accumulation in the liver, enhancing antioxidant activity, and improving overall lipid metabolism.
Moreover, we noted that increased intestinal permeability was linked to a worsening of NAFLD symptoms. With the help of cutting-edge metabolomics and transcriptomic analysis, we pinpointed the significance of vitamin B6, which may act as a metabolite produced by gut bacteria. This insight suggests a promising direction for NAFLD treatments that incorporate dietary sources of vitamin B6.
Read More
User Reviews
USERS' SCORE
Good
Based on 3 Reviews
8.4
- All Reviews
- Positive Reviews
- Negative Reviews
7.5
Improved calmness
This was recommended by my nutritionist, and since then, my sleep has improved and I've felt calmer. I’m keen to undertake another course to continue addressing my liver disease.
Read More
9
Lowers homocysteine levels
2 people found this helpful
I use this to reduce my homocysteine levels, which are linked to heart disease, including liver disease. It is essential to have the methylated versions of these vitamins.
Read More
7.5
Good for assimilation
3 people found this helpful
I purchased this remedy for my elderly father, who suffers from blood clots and liver disease. It has a pleasant taste and did not cause any adverse reactions, despite his liver issues. The dosage is good, with the active folate form allowing for better absorption of the vitamin complex. I will order more.
Read More
Frequently Asked Questions
7.5
Improved calmness
This was recommended by my nutritionist, and since then, my sleep has improved and I've felt calmer. I’m keen to undertake another course to continue addressing my liver disease.
9
Lowers homocysteine levels
2 people found this helpful
I use this to reduce my homocysteine levels, which are linked to heart disease, including liver disease. It is essential to have the methylated versions of these vitamins.
7.5
Good for assimilation
3 people found this helpful
I purchased this remedy for my elderly father, who suffers from blood clots and liver disease. It has a pleasant taste and did not cause any adverse reactions, despite his liver issues. The dosage is good, with the active folate form allowing for better absorption of the vitamin complex. I will order more.
7
We investigated how vitamin B6, produced by our gut bacteria, can impact liver disease, particularly alcohol-associated liver disease (ALD). This condition is a serious health issue, marked by various stages including fatty liver, fibrosis, and even cancer. Our research focused on whether a disruption in gut microbiota—common in people who consume alcohol heavily—could lead to lower production of vitamin B6, influencing the progression of ALD.
Using a mouse model that mimics binge drinking, we examined the differences in gut bacteria between those with ALD and those that were pair-fed (not consuming alcohol). By analyzing liver protein levels and various metabolites in the liver and plasma, we aimed to explore the role of vitamin B6 in the mechanisms behind ALD.
Our findings revealed that the altered gut microbiota in those with ALD significantly reduced vitamin B6 synthesis. This reduction seems to impair amino acid and glutathione metabolism in the liver, worsening the disease. Essentially, vitamin B6 appears to play a critical protective role in the face of ALD by helping regulate vital bodily functions. Overall, our study emphasizes the importance of gut health and vitamin B6 in managing alcohol-related liver damage.
Using a mouse model that mimics binge drinking, we examined the differences in gut bacteria between those with ALD and those that were pair-fed (not consuming alcohol). By analyzing liver protein levels and various metabolites in the liver and plasma, we aimed to explore the role of vitamin B6 in the mechanisms behind ALD.
Our findings revealed that the altered gut microbiota in those with ALD significantly reduced vitamin B6 synthesis. This reduction seems to impair amino acid and glutathione metabolism in the liver, worsening the disease. Essentially, vitamin B6 appears to play a critical protective role in the face of ALD by helping regulate vital bodily functions. Overall, our study emphasizes the importance of gut health and vitamin B6 in managing alcohol-related liver damage.
8
We explored the effects of vitamin B6 in combating nonalcoholic fatty liver disease (NAFLD) through a study that utilized a mouse model. The mice were fed a diet designed to induce NAFLD, and then we treated them with green pea hull polyphenol extract, which is rich in beneficial compounds, including vitamin B6.
Our findings revealed that vitamin B6 plays a crucial role in alleviating the symptoms of NAFLD. We observed that after the intervention with the green pea extract, the vitamin B6 levels significantly increased in the mice's livers. This surge in vitamin B6 appears to activate important signaling pathways that aid in reducing fat accumulation in the liver, enhancing antioxidant activity, and improving overall lipid metabolism.
Moreover, we noted that increased intestinal permeability was linked to a worsening of NAFLD symptoms. With the help of cutting-edge metabolomics and transcriptomic analysis, we pinpointed the significance of vitamin B6, which may act as a metabolite produced by gut bacteria. This insight suggests a promising direction for NAFLD treatments that incorporate dietary sources of vitamin B6.
Our findings revealed that vitamin B6 plays a crucial role in alleviating the symptoms of NAFLD. We observed that after the intervention with the green pea extract, the vitamin B6 levels significantly increased in the mice's livers. This surge in vitamin B6 appears to activate important signaling pathways that aid in reducing fat accumulation in the liver, enhancing antioxidant activity, and improving overall lipid metabolism.
Moreover, we noted that increased intestinal permeability was linked to a worsening of NAFLD symptoms. With the help of cutting-edge metabolomics and transcriptomic analysis, we pinpointed the significance of vitamin B6, which may act as a metabolite produced by gut bacteria. This insight suggests a promising direction for NAFLD treatments that incorporate dietary sources of vitamin B6.
7
We examined the impact of vitamin B6 on individuals suffering from primary sclerosing cholangitis (PSC), a serious liver condition. Our research involved a thorough analysis of blood samples from several distinct groups, totaling 373 PSC patients and 100 healthy individuals, using advanced testing methods to measure B6 levels.
It became clear that a significant number of people with PSC, many of whom were already diagnosed with liver disease, experience low vitamin B6 levels. Even after undergoing liver transplantation, these patients often continued to show signs of vitamin B6 deficiency. Importantly, we found that low levels of vitamin B6 were closely linked to poorer outcomes, including a decreased chance of survival without the need for liver transplantation.
Despite the connection between vitamin B6 status and disease outcomes, the study did not directly address whether vitamin B6 supplementation could yield significant benefits in treating liver disease. Nevertheless, our findings suggest that monitoring and potentially enhancing vitamin B6 levels could be an important aspect of managing PSC and improving patient outcomes. Therefore, exploring vitamin B6 supplementation or adjusting the gut microbiome might be worthwhile areas for future research to see if they can help PSC patients.
It became clear that a significant number of people with PSC, many of whom were already diagnosed with liver disease, experience low vitamin B6 levels. Even after undergoing liver transplantation, these patients often continued to show signs of vitamin B6 deficiency. Importantly, we found that low levels of vitamin B6 were closely linked to poorer outcomes, including a decreased chance of survival without the need for liver transplantation.
Despite the connection between vitamin B6 status and disease outcomes, the study did not directly address whether vitamin B6 supplementation could yield significant benefits in treating liver disease. Nevertheless, our findings suggest that monitoring and potentially enhancing vitamin B6 levels could be an important aspect of managing PSC and improving patient outcomes. Therefore, exploring vitamin B6 supplementation or adjusting the gut microbiome might be worthwhile areas for future research to see if they can help PSC patients.
References
- Shen H, Zhou L, Yang Y, Shu H, Wu D, et al. The gut microbiota-produced vitamin B6 mitigates alcohol-associated liver disease by attenuating hepatic oxidative stress damage. Hepatol Commun. 2025;9. 10.1097/HC9.0000000000000599
- Guo F, Xiong H, Tsao R, Shahidi F, Wen X, et al. Green Pea ( L.) Hull Polyphenol Extract Alleviates NAFLD through VB6/TLR4/NF-κB and PPAR Pathways. J Agric Food Chem. 2023;71:16067. 10.1021/acs.jafc.3c02337
- Braadland PR, Bergquist A, Kummen M, Bossen L, Engesæter LK, et al. Clinical and biochemical impact of vitamin B6 deficiency in primary sclerosing cholangitis before and after liver transplantation. J Hepatol. 2023;79:955. 10.1016/j.jhep.2023.05.038
- Xin Q, Dong Y, Guo W, Zhao X, Liu Z, et al. Four novel variants identified in primary hyperoxaluria and genotypic and phenotypic analysis in 21 Chinese patients. Front Genet. 2023;14:1124745. 10.3389/fgene.2023.1124745
- Lin S, Huang L, Wu Y, Huang L, Wu P, et al. Uncovering the protective mechanism of Pien-Tze-Huang in rat with alcoholic liver injury based on cytokines analysis and untargeted metabonomics. J Chromatogr B Analyt Technol Biomed Life Sci. 2023;1217:123626. 10.1016/j.jchromb.2023.123626
- Mei M, Liu D, Tang X, You Y, Peng B, et al. Vitamin B6 Metabolic Pathway is Involved in the Pathogenesis of Liver Diseases via Multi-Omics Analysis. J Hepatocell Carcinoma. 2022;9:729. 10.2147/JHC.S370255
- Huang C, Luo Y, Liu Y, Liu J, Chen Y, et al. DNA hypermethylation-induced suppression of ALKBH5 is required for folic acid to alleviate hepatic lipid deposition by enhancing autophagy in an ATG12-dependent manner. J Nutr Biochem. 2025. 10.1016/j.jnutbio.2025.109870
- Christensen KE, Faquette ML, Leclerc D, Keser V, Luan Y, et al. Folic Acid and Methyltetrahydrofolate Supplementation in the Mouse Model with Hepatic Steatosis. Nutrients. 2024;17. 10.3390/nu17010082
- Zhu J, Liao X, Du L, Lv P, Deng J. Associations of serum folate and vitamin B levels with all-cause mortality among patients with metabolic dysfunction associated steatotic liver disease: a prospective cohort study. Front Endocrinol (Lausanne). 2024;15:1426103. 10.3389/fendo.2024.1426103
- India-Aldana S, Midya V, Betanzos-Robledo L, Yao M, Alcalá C, et al. Impact of metabolism-disrupting chemicals and folic acid supplementation on liver injury and steatosis in mother-child pairs. J Hepatol. 2024. 10.1016/j.jhep.2024.11.050
- Dong J, Li Z, Wang C, Zhang R, Li Y, et al. Dietary folate intake and all-cause mortality and cardiovascular mortality in American adults with non-alcoholic fatty liver disease: Data from NHANES 2003 to 2018. PLoS One. 2024;19:e0314148. 10.1371/journal.pone.0314148
- Li Y, Shu J, Tan P, Dong X, Zhang M, et al. Genetic variants in folate metabolism-related genes, serum folate and hepatocellular carcinoma survival: the Guangdong Liver Cancer Cohort study. Br J Nutr. 2024;132:1411. 10.1017/S0007114524001776
- Xu W, Wang Y, Cui S, Zheng Q, Lin Y, et al. Methylcobalamin protects against liver failure via engaging gasdermin E. Nat Commun. 2025;16:1233. 10.1038/s41467-024-54826-6
- Abu-Zahab ZA, Qureshi H, Adham GM, Elzefzafy WM, Zalam SS, et al. Frequency of comorbid diseases with high serum Vitamin B12 levels in patients attending King Salman Medical City (KSAMC), at Madinah. Int J Health Sci (Qassim). 2025;19:15.
- Espina S, Casas-Deza D, Bernal-Monterde V, Royo-Esteban A, García-Sobreviela MP, et al. Unraveling the Association of Liver Steatosis and Fibrosis with Vitamin B12: A Cross-Sectional Study. Metabolites. 2024;14. 10.3390/metabo14110618
- Roy A, Trigun SK. The restoration of hippocampal nerve de-myelination by methylcobalamin relates with the enzymatic regulation of homocysteine level in a rat model of moderate grade hepatic encephalopathy. J Biochem Mol Toxicol. 2024;38:e23695. 10.1002/jbt.23695
- Pai SL, Torp KD, Insignares VC, DeMaria S, Giordano CR, et al. Use of hydroxocobalamin to treat intraoperative vasoplegic syndrome refractory to vasopressors and methylene blue during liver transplantation. Clin Transplant. 2024;38:e15271. 10.1111/ctr.15271
- Liu K, Chen Y, Chen J, Chen W, Sun X, et al. Genetically determined circulating micronutrients and the risk of nonalcoholic fatty liver disease. Sci Rep. 2024;14:1105. 10.1038/s41598-024-51609-3
- Boachie J, Zammit V, Saravanan P, Adaikalakoteswari A. Metformin Inefficiency to Lower Lipids in Vitamin B12 Deficient HepG2 Cells Is Alleviated via Adiponectin-AMPK Axis. Nutrients. 2023;15. 10.3390/nu15245046
- Oula JO, Mose JM, Waiganjo NN, Chepukosi KW, Mitalo NS, et al. Vitamin B12 blocked Trypanosoma brucei rhodesiense-driven disruption of the blood brain barrier, and normalized nitric oxide and malondialdehyde levels in a mouse model. Parasitol Int. 2023;96:102775. 10.1016/j.parint.2023.102775
- Ujianti I, Sianipar IR, Prijanti AR, Hasan I, Arozal W, et al. Effect of Roselle Flower Extract ( Linn.) on Reducing Steatosis and Steatohepatitis in Vitamin B12 Deficiency Rat Model. Medicina (Kaunas). 2023;59. 10.3390/medicina59061044
- Ahmed Mohammed R, Fadheel QJ. Hepatoprotective Effect of Vitamin B12 in Acetaminophen Induce Hepatotoxicity in Male Rats. Arch Razi Inst. 2023;78:419. 10.22092/ARI.2022.359353.2408
