Evidence map›Paper›PMID 37299482›Full record

ReviewNutrients2023

Type 2 Diabetes Mellitus and Liver Disease: Across the Gut-Liver Axis from Fibrosis to Cancer.

Vittoria Manilla, Francesco Santopaolo, Antonio Gasbarrini, Francesca Romana Ponziani

Open access · goldAbstract readReview
In one paragraph

Review in Nutrients, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 3% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Guideline
  2. Article
  3. Review
  4. Insulin Resistance and Inflammation.International journal of molecular sciences · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Pharmaceuticals (Basel, Switzerland) · 2024
    Article
  18. Review
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

4 authors at 2 institutions in 1 country.

Vittoria ManillaDigestive Disease Center-CEMAD, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy.
Francesco SantopaoloDigestive Disease Center-CEMAD, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy.ORCID 0000-0002-1773-1171
Antonio GasbarriniDigestive Disease Center-CEMAD, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy.ORCID 0000-0002-6230-1779
Francesca Romana PonzianiDigestive Disease Center-CEMAD, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy.ORCID 0000-0002-5924-6238
Agostino Gemelli University Polyclinic · ITUniversità Cattolica del Sacro Cuore · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetes mellitus is a widespread disease worldwide, and is one of the cornerstones of metabolic syndrome. The existence of a strong relationship between diabetes and the progression of liver fibrosis has been demonstrated by several studies, using invasive and noninvasive techniques. Patients with type 2 diabetes mellitus (T2DM) and nonalcoholic fatty liver disease (NAFLD) show faster progression of fibrosis than patients without diabetes. Many confounding factors make it difficult to determine the exact mechanisms involved. What we know so far is that both liver fibrosis and T2DM are expressions of metabolic dysfunction, and we recognize similar risk factors. Interestingly, both are promoted by metabolic endotoxemia, a low-grade inflammatory condition caused by increased endotoxin levels and linked to intestinal dysbiosis and increased intestinal permeability. There is broad evidence on the role of the gut microbiota in the progression of liver disease, through both metabolic and inflammatory mechanisms. Therefore, dysbiosis that is associated with diabetes can act as a modifier of the natural evolution of NAFLD. In addition to diet, hypoglycemic drugs play an important role in this scenario, and their benefit is also the result of effects exerted in the gut. Here, we provide an overview of the mechanisms that explain why diabetic patients show a more rapid progression of liver disease up to hepatocellular carcinoma (HCC), focusing especially on those involving the gut-liver axis.

Indexed as

Carcinoma, HepatocellularDiabetes Mellitus, Type 2Liver NeoplasmsNon-alcoholic Fatty Liver DiseaseDysbiosisFibrosisHumansLiverLiver Cirrhosischolangiocarcinomadiabetesgut–liver axishepatocellular carcinoma (HCC)insulin resistance (IR)liver fibrosisliver sinusoid endothelial cell (LSEC)lypopolisaccharides (LPS)mitochondrianon-alcoholic fatty liver disease (NAFLD)

Identifiers

PMID37299482
PMCPMC10255218
OpenAlexW4378714251

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.