Evidence map›Paper›PMID 24468786›Full record

ArticleAntimicrobial agents and chemotherapy2014

An altered Mycobacterium tuberculosis metabolome induced by katG mutations resulting in isoniazid resistance.

Du Toit Loots

Open access · bronzeAbstract read
In one paragraph

Article in Antimicrobial agents and chemotherapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. M. tuberculosis AlkX Encoded byMicrobiology spectrum · 2022
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Microbiology spectrum · 2019
    Review
  14. Article
  15. Panomics for Precision Medicine.Trends in molecular medicine · 2018
    Review
  16. Review
  17. Metabolomics: Applications and Promise in Mycobacterial Disease.Annals of the American Thoracic Society · 2015
    Review
  18. Mycobacterium tuberculosis metabolism.Cold Spring Harbor perspectives in medicine · 2014
    Review
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Du Toit LootsCentre for Human Metabonomics, School for Physical and Chemical Sciences, North-West University, Potchefstroom, South Africa.
North-West University · ZA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The most common form of drug resistance found in tuberculosis (TB)-positive clinical samples is monoresistance to isoniazid. Various genomics and proteomics studies to date have investigated this phenomenon; however, the exact mechanisms relating to how this occurs, as well as the implications of this on the TB-causing organisms function and structure, are only partly understood. Considering this, we followed a metabolomics research approach to identify potential new metabolic pathways and metabolite markers, which when interpreted in context would give a holistic explanation for many of the phenotypic characteristics associated with a katG mutation and the resulting isoniazid resistance in Mycobacterium tuberculosis. In order to achieve these objectives, gas chromatography-time of flight mass spectrometry (GCxGC-TOFMS)-generated metabolite profiles from two isoniazid-resistant strains were compared to a wild-type parent strain. Principal component analyses showed clear differentiation between the groups, and the metabolites best describing the separation between these groups were identified. It is clear from the data that due to a mutation in the katG gene encoding catalase, the isoniazid-resistant strains experience increased susceptibility to oxidative stress and have consequently adapted to this by upregulating the synthesis of a number of compounds involved in (i) increased uptake and use of alkanes and fatty acids as a source of carbon and energy and (ii) the synthesis of a number of compounds directly involved in reducing oxidative stress, including an ascorbic acid degradation pathway, which to date hasn't been proposed to exist in these organisms.

Indexed as

Antitubercular AgentsBacterial ProteinsIsoniazidMetabolomeMutationMycobacterium tuberculosisOxidative StressAntitubercular AgentsBacterial ProteinsIsoniazid

Identifiers

PMID24468786
PMCPMC4023710
OpenAlexW2054695402

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.