BHMT

Last update 08 May 2025

Basic Info

Synonyms

betaine--homocysteine S-methyltransferase, Betaine--homocysteine S-methyltransferase 1, BHMT

+ [1]

Introduction

Involved in the regulation of homocysteine metabolism. Converts betaine and homocysteine to dimethylglycine and methionine, respectively. This reaction is also required for the irreversible oxidation of choline.

100 Clinical Results associated with BHMT

100 Translational Medicine associated with BHMT

0 Patents (Medical) associated with BHMT

397

Literatures (Medical) associated with BHMT

01 Dec 2025·Molecular Biology Reports

The complex role of glycine N-methyltransferase in metabolism-a review

Review

Author: Islam, Md Numan ; Ahmed, Tanvir ; Suzauddula, Md

BACKGROUNDGlycine N-methyltransferase (GNMT) is an enzyme predominantly found in the liver, playing a crucial role in various metabolic pathways. GNMT is involved in transmethylation, transsulfuration, one-carbon metabolism, energy metabolism, and DNA methylation. Deletion or Knockdown of GNMT influences the expression of several key metabolic enzymes by accumulating S-adenosylmethionine (SAM). Dysregulation of GNMT and these metabolic enzymes can lead to metabolic dysfunction and chronic diseases.OBJECTIVETo provide a comprehensive review of the impact of Glycine N-methyltransferase (GNMT) on metabolism, focusing on its epigenetic and genetic mechanisms, its role in metabolic pathways, and its association with chronic diseases.RESULTSGNMT is highly expressed in the liver and exerts direct and indirect effects on various metabolic pathways, including transmethylation, transsulfuration, one-carbon metabolism, energy metabolism, and global DNA methylation. Current understanding suggests that GNMT operates through both epigenetic and genetic mechanisms, influencing the expression of key metabolic enzymes such as BHMT, NNMT, PEMT, DNMTs, CBS, and MTHFR through the accumulation of S-adenosylmethionine. Dysregulation of these proteins not only affects metabolic function but also contributes to the development of several chronic diseases. Furthermore, the level of GNMT protein has been directly linked to non-alcoholic fatty liver disease, with its function being gender, age, and organ specific. At the same time, GNMT and disease progression correlate, dietary supplementation and pharmacological approaches have shown promise in controlling GNMT levels.CONCLUSIONGNMT plays a multifaceted role in metabolism, influencing various pathways and contributing to chronic disease development. Understanding its mechanisms and interactions opens avenues for targeted dietary and pharmacological therapies to manage GNMT-related metabolic dysfunction.

01 May 2025·Hepatology

LncRNA H19 promoted alcohol-associated liver disease through dysregulation of alternative splicing and methionine metabolism

Article

Author: Thoudam, Themis ; Ma, Jing ; Huda, Nazmul ; Wang, Li ; Sun, Zhaoli ; Jiang, Yanchao ; Han, Sen ; Yang, Zhihong ; Liangpunsakul, Suthat ; Kusumanchi, Praveen ; Gao, Hui

Background and Aims:Long noncoding RNAs constitute a significant portion of the human genome. Among these, lncRNA H19, initially identified for its high expression during fetal development followed by a decline in the liver postnatally, re-emerges in various liver diseases. However, its specific role in alcohol-associated liver disease (ALD) remains unclear.Approach and Results:Elevated H19 levels were detected in peripheral blood and livers of patients with alcohol-associated cirrhosis and hepatitis, as well as in livers of ethanol-fed mice. Hepatic overexpression of H19 exacerbated ethanol-induced liver steatosis and injury. Metabolomics analysis revealed decreased methionine levels in H19-overexpressed mouse livers, attributable to H19-mediated inhibition of betaine homocysteine methyltransferase (BHMT), a crucial enzyme in methionine synthesis. H19 regulated BHMT alternative splicing through polypyrimidine tract-binding protein 1 (PTBP1), resulting in a reduced Bhmt protein-coding variant. The maternally specific knockout of H19 (H19 Mat+/− ) or liver-specific knockout of the H19 differentially methylated domain (H19DMD Hep−/− ) in ethanol-fed mice upregulated BHMT expression and ameliorated hepatic steatosis. Furthermore, BHMT restoration counteracted H19-induced ethanol-mediated hepatic steatosis.Conclusions:This study identifies a novel mechanism whereby H19, via PTBP1–mediated BHMT regulation, influences methionine metabolism in ALD. Targeting the H19-PTBP1-BHMT pathway may offer new therapeutic avenues for ALD.

01 Mar 2025·Rapid Communications in Mass Spectrometry

Integrative multi‐omics reveals the mechanism of ulcerative colitis treated with Ma‐Mu‐Ran antidiarrheal capsules

Article

Author: Zhang, Dongning ; Chen, Pengyu ; Han, Lintao ; Huang, Fang ; Ye, Yan ; Wen, Yuxin ; Wang, Qiong ; Huang, Ping ; Zheng, Sili ; Wang, Shanshan ; Jiang, Qi ; Liu, Jiajing ; Huang, Zhuang ; Duan, Bailu ; Li, Jingjing ; Huang, Hailing

RationaleUlcerative colitis (UC) is a chronic inflammatory gastrointestinal disease typically coexisting with intestinal microbiota dysbiosis, oxidative stress, and an inflammatory response. Although its underlying mechanism of action is unclear, Ma‐Mu‐Ran Antidiarrheal Capsules (MMRAC) have demonstrated significant therapeutic efficacy for UC.MethodsThe mechanism of action of MMRAC in the treatment of UC model was investigated by combining metabolomics, transcriptomics, and intestinal microbiota detection techniques.ResultsThe high‐dose group of MMRAC was determined as the best therapeutic dose by pathological changes and biochemical indexes. Transcriptome analysis revealed that 360 genes were differentially altered after MMRAC treatment. Metabolomic analysis using colon tissue yielded 14 colon tissue metabolites with significant differences. Intestinal flora analysis showed that 26 major microorganisms were identified at the genus level.ConclusionsBased on a thorough multi‐omics analysis of transcriptomics, metabolomics, and gut flora, it was determined that MMRAC regulated cysteine and methionine metabolism, arginine biosynthesis, and sphingolipid metabolism and their respective genes BHMT, PHGDH, iNOS, and SPHK1, which in turn served to inhibit UC‐generated inflammatory responses and oxidative stress. Additionally, MMRAC regulated the abundance of Coprococcus, Helicobacter, Sutterella, Paraprevotella, and Roseburia in the intestinal tracts of UC mice, which was regulated toward normal levels, thereby restoring normal intestinal function.

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