ReviewExpert opinion on drug metabolism & toxicology2010
The biochemical and toxicological significance of hypermethionemia: new insights and clinical relevance.
Review in Expert opinion on drug metabolism & toxicology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 22 citations in OpenAlex.
- Article
- Hepatic and extrahepatic metabolic modulation in hbv-related decompensated cirrhosis and acute-on-chronic liver failure.Virulence · 2024Article
- Plasma Amino Acid Concentration in Obese Horses with/without Insulin Dysregulation and Laminitis.Animals : an open access journal from MDPI · 2022Article
- Dynamic changes of metabolic characteristics in neonatal intrahepatic cholestasis caused by citrin deficiency.Frontiers in molecular biosciences · 2022Article
- Methionine dietary supplementation potentiates ionizing radiation-induced gastrointestinal syndrome.American journal of physiology. Gastrointestinal and liver physiology · 2020Article
- Mudd's disease (MAT I/III deficiency): a survey of data for MAT1A homozygotes and compound heterozygotes.Orphanet journal of rare diseases · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
importance of the fieldDisrupted l-methionine (Met) metabolism can lead to hepatic, neurological and cardiovascular dysfunction in humans. Aberrant methyl group flux likely contributes to the development of these pathologies, but when patients also become hypermethionemic, additional toxicological mechanisms may be relevant. AREAS COVERED IN THIS REVIEW: Following a discussion of the causes of hypermethionemia in humans, evidence for the toxicological roles and clinical significance of the Met transmethylation (TM), transamination (TA) and sulfoxidation (SO) pathways will be presented. WHAT THE READER WILL GAIN: Recent data from freshly isolated mouse hepatocytes (FIMHs) confirmed previous in vivo results in rodents that Met TM is a detoxification pathway while Met TA leads to toxicity. Gender-related differences in Met accumulation and metabolism in FIMHs correlated with gender differences in toxicity. Data obtained from FIMHs also implicated Met SO in Met metabolism and toxicity. Currently, little is known about the mechanisms and biological significance of Met sulfoxidation in humans. TAKE HOME MESSAGE: In hypermethionemic patients, clinical and dietary interventions should focus on increasing Met TM and decreasing Met TA and SO. Novel biomarkers of hypermethionemia in humans that correlate with pathological end points are needed to better understand the impact of the condition.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.