Evidence map›Paper›PMID 31573841›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2019

Amelioration of metabolic syndrome by metformin associates with reduced indices of low-grade inflammation independently of the gut microbiota.

Aneseh Adeshirlarijaney, Jun Zou, Hao Q Tran, Benoit Chassaing, Andrew T Gewirtz

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 2 pooled it
2.3field-weighted citation impact, top 11% 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

31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Metformin and Myo-Inositol: A Comparative Analysis.Gynecologic and obstetric investigation · 2026
    Review
  5. Article
  6. Article
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  9. Specific Alternation of Gut Microbiota and the Role ofJournal of microbiology and biotechnology · 2024
    Article
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  13. Review
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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

5 authors at 1 institution in 1 country.

Aneseh AdeshirlarijaneyInstitute for Biomedical Sciences, Georgia State University, Atlanta, Georgia.
Jun ZouInstitute for Biomedical Sciences, Georgia State University, Atlanta, Georgia.
Hao Q TranInstitute for Biomedical Sciences, Georgia State University, Atlanta, Georgia.
Benoit ChassaingInstitute for Biomedical Sciences, Georgia State University, Atlanta, Georgia.ORCID 0000-0002-4285-769X
Andrew T GewirtzInstitute for Biomedical Sciences, Georgia State University, Atlanta, Georgia.
Georgia State University · US

Funding

Pathophysiology of TLR5KO ColitisR01DK083890 · NIDDK · GEORGIA STATE UNIVERSITY · PI GEWIRTZ, ANDREW T · 2010 to 2023
$5.0M
NIDDK NIH HHS R01 DK083890
6 · The paper itself

Abstract

Metformin beneficially impacts several aspects of metabolic syndrome including dysglycemia, obesity, and liver dysfunction, thus making it a widely used frontline treatment for early-stage type 2 diabetes, which is associated with these disorders. Several mechanisms of action for metformin have been proposed, including that it acts as an anti-inflammatory agent, possibly as a result of its impact on intestinal microbiota. In accord with this possibility, we observed herein that, in mice with diet-induced metabolic syndrome, metformin impacts the gut microbiota by preventing its encroachment upon the host, a feature of metabolic syndrome in mice and humans. However, the ability of metformin to beneficially impact metabolic syndrome in mice was not markedly altered by reduction or elimination of gut microbiota, achieved by the use of antibiotics or germfree mice. Although reducing or eliminating microbiota by itself suppressed diet-induced dysglycemia, other features of metabolic syndrome including obesity, hepatic steatosis, and low-grade inflammation remained suppressed by metformin in the presence or absence of gut microbiota. These results support a role for anti-inflammatory activity of metformin, irrespective of gut microbiota, in driving some of the beneficial impacts of this drug on metabolic syndrome.

Indexed as

AmpicillinAnimalsAnti-Bacterial AgentsDiet, High-FatFatty LiverGastrointestinal MicrobiomeGerm-Free LifeHyperglycemiaHypoglycemic AgentsInflammationLiverMetabolic SyndromeMetforminMiceNeomycinObesityAmpicillinAnti-Bacterial AgentsHypoglycemic AgentsMetforminNeomycinantibioticsgerm freehigh-fat dietmetabolic syndromemetforminmicrobiotasteatosis

Identifiers

PMID31573841
PMCPMC6962505
OpenAlexW2978635276

What OpenQuestion holds

Texttitle and abstract
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.