Ask about this productRelated genes to: FMO3 Blocking Peptide
- Gene:
- FMO3 NIH gene
- Name:
- flavin containing monooxygenase 3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-10-16
- Date modifiied:
- 2018-05-03
Related products to: FMO3 Blocking Peptide
Related articles to: FMO3 Blocking Peptide
- Metabolic bariatric surgery, such as vertical sleeve gastrectomy (VSG), is the most effective treatment for obesity, yet the molecular mechanisms remain incompletely defined. This study aims to explore the role of hepatic flavin monooxygenase 3 (FMO3) in the metabolic improvements of VSG. - Source: PubMed
Publication date: 2026/08/05
Yan HaiCao ChongTan XiaozhuoHuang XianjueLiu YanyangChu YuxiaoHe MengchengYao QiyuanHua RongShao Yikai - High-fat/choline diets can induce the production of the enterogenous metabolite trimethylamine--oxide (TMAO). TMAO is synthesized from its precursor trimethylamine (TMA), which is generated choline cleavage catalyzed by choline trimethylamine-lyase/choline TMA-lyase-activating enzyme (CutC/D) expressed by gut microbes; subsequently, TMA is oxidized to TMAO by flavin-containing monooxygenase 3 (FMO3) in the liver. While epigallocatechin gallate (EGCG) is well recognized for its gut microbiota-remodeling capacity, how it modulates TMA/TMAO metabolism through this pathway, along with the time-dependent effectiveness of EGCG intervention, remains to be elucidated. We conducted animal experiments to evaluate the inhibitory effect of time-dependent EGCG intervention on TMA/TMAO production induced by high-fat/choline diets in mice. We further identified gut bacterial strains associated with TMA levels using metagenomics and machine learning techniques, and verified the underlying mechanisms through anaerobic culture and molecular simulations. Results demonstrated EGCG significantly reduced TMA/TMAO levels in mice by regulating the choline-CutC/D-FMO3 axis. Specifically, exhibited a positive correlation with CutC enzyme activity, while showed a negative correlation with TMA levels. Mechanistically, EGCG exerted a direct bacteriostatic effect on by disrupting its cell membrane structure and inhibiting its CutC enzyme activity. Meanwhile, EGCG significantly enriched , with the abundance of this strain peaking after long-term intervention. Although does not directly degrade TMA, it indirectly reduces TMA levels by inhibiting the growth of . Long-term continuous supplementation with EGCG yielded the optimal inhibitory effect on TMA/TMAO production. Hence, EGCG exerts its function primarily through a dual mechanism: directly inhibiting the growth and CutC enzyme activity of the TMA-producing bacterium , and indirectly antagonizing by promoting the proliferation of the beneficial bacterium . This study provides novel theoretical insights into the mechanism by which EGCG alleviates TMA/TMAO metabolic disorders induced by high-fat/choline diets gut microbiota modulation. - Source: PubMed
Publication date: 2026/07/30
Wang ZhuoGao QianyaLi ShanshanFang ZhengfengHu LiangLi RanZeng ZhenLiu YuntaoLi ChengChen Hong - Flavin-containing monooxygenase 3 (FMO3) oxidizes trimethylamine (TMA), a gut-derived metabolite of dietary substrates such as choline and betaine, into trimethylamine--oxide (TMAO), which has been linked to cardiometabolic and renal diseases. We examined whether two common genetic variants, p.Glu158Lys (E158K, rs2266782) and p.Glu308Gly (E308G, rs2266780), were associated with circulating TMA and TMAO in a sub-study of a randomized clinical trial incorporating dietary substrate loads (136 fasting samples from four visits). Each Gly308 allele was associated with approximately 18% lower plasma TMAO concentrations and accounted for approximately one-third of baseline ln(TMAO) variation, independent of rs2266782 and robust to adjustment for estimated glomerular filtrate rate. In contrast, plasma TMA concentrations did not differ by genotype. No consistent genotype effects were observed for blood pressure, although systolic blood pressure showed a genotype × treatment interaction without main genotype or treatment effects. Given the small sample size and sparse genotype representation, these findings should be interpreted as exploratory and may reflect variation in TMA oxidation efficiency. In conclusion, this initial study suggests that individuals carrying the Gly308 variant exhibit lower circulating TMAO without detectable increases in TMA, consistent with preserved short-term substrate handling under controlled conditions and motivating further investigation of the TMA-TMAO pathway in larger, genotype-balanced cohorts. - Source: PubMed
Publication date: 2026/07/13
Tang JustinZaretsky Joshua ALabajo Jaden DShaqo AbirDakroub HamzaShelp Gia VPoole Elizabeth MBurns Sarah ECho Clara E - : The aim of this study is to evaluate the relationship between adherence to the Mediterranean diet and intestinal microbiota metabolite trimethylamine N-oxide (TMAO) levels, systemic inflammation markers, and oxidative stress parameters in patients with metabolic dysfunction-associated steatotic liver disease (MASLD). : MASLD patients whose fatty liver and fibrosis severity were determined with FibroScan and a healthy control group were included in the study. In addition to the routine biochemical parameters, serum TMAO levels, inflammatory cytokines (IL-6, IL-10, TNF-α), and oxidative stress indicators (malondialdehyde, glutathione, and MDA/GSH ratio) of all participants were measured. In comparing these parameters between fibrosis groups, adjustment for potential confounding variables (age, BMI, sex, comorbidity, relevant medication use, MEDAS score, and physical activity) was performed. Following anthropometric evaluations, the adherence levels of the participants to the Mediterranean diet were determined by the Mediterranean Diet Adherence Screening Scale (MEDAS), and their physical activity levels were determined through the International Physical Activity Questionnaire-Short Form (IPAQ-SF). Individuals diagnosed with MASLD had significantly lower adherence to the Mediterranean diet and lower physical activity levels compared with healthy controls. Among the inflammatory parameters, IL-6 levels were significantly higher in the advanced fibrosis group than in the early-stage and significant fibrosis groups, while TNF-α levels were significantly higher in the advanced fibrosis group than in the early fibrosis group. No significant differences were observed among the groups in TMAO, IL-10, GSH levels, or the MDA/GSH ratio; however, among the oxidative stress markers, MDA levels were significantly higher in the early fibrosis group than in the significant fibrosis group. In MASLD patients, fibrosis severity was associated with alterations in TMAO, inflammatory, and oxidative stress markers, with increased TNF-α and IL-6 levels reflecting a high inflammatory burden as fibrosis progressed. Lower TMAO levels in fibrosis groups likely reflect reduced hepatic FMO3 activity, lower fish intake, and medication use, while elevated MDA levels in early-stage fibrosis suggest that lipid peroxidation may be more prominent in the initial phases of disease. Mediterranean diet adherence and physical activity were inversely associated with pro-inflammatory markers and MASLD severity, being highest in the control group, suggesting a potential protective role for these lifestyle factors in MASLD progression. - Source: PubMed
Publication date: 2026/07/09
Kazdal Saibe MerveArpa MedeniKeklikkiran ÇağlayanYücecan Sevinç - Male infertility refers to the inability of a male partner to contribute to pregnancy after 12 months or more of regular unprotected intercourse. It is frequently associated with impaired spermatogenesis, and many cases cannot be completely explained by genetic, inflammatory, endocrine, or environmental factors. Trimethylamine N-oxide (TMAO) is generated when gut bacteria convert dietary choline, L-carnitine, and betaine into trimethylamine (TMA), which is oxidized in the liver mainly by flavin-containing monooxygenase 3 (FMO3). This focused review evaluates current evidence on TMAO and impaired spermatogenesis within the gut-testis axis. The rationale is biologically plausible because sperm motility depends on coordinated glycolytic and mitochondrial energy metabolism, whereas Leydig cell steroidogenesis depends on mitochondrial cholesterol transport and redox balance. Human observational studies associate TMAO with asthenozoospermia and Leydig cell-related markers, particularly insulin-like peptide 3 (INSL3), while mouse studies suggest testicular injury and reduced spermatogenesis after TMAO-related exposure. The Hippo/Yes-associated protein (YAP)-mitochondria-steroidogenic acute regulatory protein (StAR) axis has been proposed as one possible mechanism, but direct reproductive tract exposure, blood-testis barrier kinetics, and human validation remain unresolved. Overall, TMAO should be considered as a candidate metabolic mediator and not a proven causal factor or therapeutic target in male infertility. - Source: PubMed
Publication date: 2026/07/06
Zhang XinyangLuo JialinZhang XiangYang FangZhang XiaojinYu XujunDong Liang