Ask about this productRelated genes to: BHMT antibody
- Gene:
- BHMT NIH gene
- Name:
- betaine--homocysteine S-methyltransferase
- Previous symbol:
- -
- Synonyms:
- BHMT1
- Chromosome:
- 5q14.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-06-09
- Date modifiied:
- 2014-11-19
Related products to: BHMT antibody
Related articles to: BHMT antibody
- Betaine acts as a methyl donor and has been proposed as a potential substitute for methionine (Met) to reduce feed costs. This study aimed to investigate the optimal replacement value of betaine for dietary Met in broilers aged 22 to 42 days. A total of 1,440 male broilers were randomly divided into 6 treatments (6 replicates/pen). The positive control (PC) received a standard diet (0.53% Met), while the negative control (NC) received a low-Met diet (0.33% Met) with 2000 mg/kg betaine. Four additional groups received the NC diet supplemented with 0.05%, 0.10%, 0.15%, or 0.20% Met. Data were analyzed using one-way ANOVA and three regression models. Results indicated that Met deficiency significantly impaired growth performance: final body weight (BW) decreased from 1696 g (PC) to 1604 g (NC) (P < 0.001), while the feed-to-gain ratio (F/G) increased from 1.87 to 2.01. No significant differences were observed in slaughter performance (P > 0.05). Regarding metabolism, the NC group exhibited significantly elevated serum homocysteine (19.42 vs. 7.94 μmol/L) and hepatic ALT activity (11.77 vs. 4.35 U/g prot), alongside reduced hepatic BHMT activity (17.47 vs. 103.14 ng/mg prot, P < 0.001). Furthermore, Met deficiency downregulated the mRNA expression of genes related to one-carbon metabolism and intestinal tight junctions (relative expression ∼0.20 vs. 1.00 in PC, P < 0.05). Supplementation with 0.10% Met restored these parameters to levels statistically equivalent to the PC group. One-slope straight broken line and two-slope straight broken line regression analysis of the F/G ratio (R2 = 0.8598) determined the optimal replacement dose to be 0.1474% Met, corresponding to a 27.81% substitution efficiency. - Source: PubMed
Publication date: 2026/05/08
Wang HengLiu LinHe XiPeng BinBian Guozhi - Disturbances in one-carbon metabolism and homocysteine (Hcy) regulation have been implicated in Alzheimer's disease (AD) and Parkinson's disease (PD), yet direct evidence from human brain tissue and the contribution of genetic variation remain limited. We investigated whether B-vitamin-related metabolic deficits and polymorphisms in one-carbon metabolism pathways contribute to cognitive impairment in AD and PD. - Source: PubMed
Publication date: 2026/04/24
Kalecký KarelCastañeda-Gill JessicaPatel SharlinBottiglieri Teodoro - Betaine-homocysteine methyltransferase (BHMT) is an enzyme involved in one-carbon metabolism and plays a crucial role in maintaining liver health. In this study, we investigated the impact of liver-specific deletion of BHMT on liver dysfunction using a mouse model. We generated BHMT floxed mice and bred them with albumin Cre to generate liver-specific BHMT knockout (BHMT LKO) mice. Liver tissues harvested from six-month-old chow-fed BHMT floxed and LKO mice were characterized through histological, biochemical, and molecular analyses. BHMT LKO mice displayed a complete loss of hepatic expression of BHMT mRNA, protein and enzyme activity. Histopathological analysis revealed the development of hepatic steatosis in BHMT LKO mice compared to the floxed mice. These morphological changes were supported by biochemical analysis showing elevated levels of hepatic triglycerides in conjunction with a profound decrease in the methylation potential (i.e., reduced S-adenosylmethionine (SAM): S-adenosylhomocysteine (SAH) ratio), which was mainly driven by a six- to sevenfold increase in SAH levels. BHMT LKO mice also exhibited increased lipid peroxidation and lysosomal dysfunction compared to floxed mice. Early signs of inflammation were seen in the livers of BHMT LKO mice of both sexes, as evident from significant increase in CD68-positive cells and interleukin 1β levels. Additionally, there was a moderate increase in fibrosis, as evidenced by the upregulated expression of α-smooth muscle actin and collagen II levels and the histological assessment of picrosirius red-stained liver sections of BHMT LKO mice of both sexes compared to their respective counterparts. These findings demonstrate that hepatic BHMT deficiency promotes lipid accumulation, lysosomal/proteasomal dysfunction, and early inflammatory and fibrotic changes in the liver by reducing the methylation potential. Collectively, our results underscore BHMT as a critical regulator of liver homeostasis and a potential therapeutic target in liver-related disorders. - Source: PubMed
Publication date: 2026/04/20
Rajamanickam RamachandranPerumal Sathish KumarBellamkonda RameshMahalingam SundararajanFisher Kurt WQuadros RolenGurumurthy Channabasavaiah BArumugam Madan KumarRasineni KarunaKharbanda Kusum K - Metabolic dysfunction-associated steatohepatitis (MASH) is associated with increased expression of peroxisome proliferator-activated receptor gamma (PPARγ, ) and reduced expression of genes involved in methionine metabolism in the liver. The nuclear receptor PPARγ is activated by fatty acids, and the knockout of in hepatocytes ( ) reduced the negative effects of MASH on methionine metabolism. Here, we sought to determine whether hepatocyte is required for the transcriptional regulation of genes involved in hepatic methionine metabolism in conditions with altered fatty acid flux to the liver: fasting, refeeding, and high-fat diet (HFD)-induced obesity/steatosis. Fasting induced liver steatosis and increased the expression of key genes involved in the methionine metabolism in the liver, while 6h-refeeding reversed these effects and reduced the expression of phosphatidylethanolamine N-methyltransferase ( and cystathionine beta synthase (. Overall, fasting and refeeding did not alter hepatocyte expression nor affected fasting and refeeding-mediated regulation of methionine metabolism gene expression. Diet-induced steatosis reduced hepatic expression in control (-intact) mice, and the thiazolidinedione (TZD)-mediated activation of PPARγ in diet-induced obese control (-intact) mice reduced the expression of betaine homocysteine S-methyltransferase ( and . However, diet-induced steatosis increased hepatocyte expression, and blocked the negative effects of HFD and TZD on hepatic methionine metabolism. The PPARγ-dependent reduction of hepatic and expression was confirmed in mouse primary hepatocytes. Taken together, hepatocyte may serve as a negative regulator of hepatic methionine metabolism in diet-induced obese mice and these actions could contribute to promoting the onset of MASH. - Source: PubMed
Publication date: 2026/03/27
Hawro IzabelaLee Samuel MKineman Rhonda DCordoba-Chacon Jose - - Source: PubMed
Publication date: 2026/03/30
Zhou HaiyanZhu TaoXie ShuningZhao YitongWang YanqiaoQin Jing