Evidence mapPaperPMID 36051336Full record

ArticleWorld journal of gastroenterology2022

Impact of sodium glucose cotransporter-2 inhibitors on liver steatosis/fibrosis/inflammation and redox balance in non-alcoholic fatty liver disease.

Francesco Bellanti, Aurelio Lo Buglio, Michał Dobrakowski, Aleksandra Kasperczyk, Sławomir Kasperczyk, Palok Aich, Shivaram P Singh, Gaetano Serviddio, Gianluigi Vendemiale

Open access · greenAbstract read
In one paragraph

Article in World journal of gastroenterology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 2 pooled it
7.0field-weighted citation impact, top 2% 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

27 citing papers in PubMed, 2 syntheses or guidelines pooled it, 50 citations in OpenAlex.

  1. Pooled it
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  18. Fatty liver index (FLI): more than a marker of hepatic steatosis.Journal of physiology and biochemistry · 2024
    Review
  19. Article
  20. The Ketogenic Effect of SGLT-2 Inhibitors-Beneficial or Harmful?Journal of cardiovascular development and disease · 2023
    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

9 authors at 2 institutions in 2 countries.

Francesco BellantiDepartment of Medical and Surgical Sciences, University of Foggia, Foggia 71122, Italy. francesco.bellanti@unifg.it.
Aurelio Lo BuglioDepartment of Medical and Surgical Sciences, University of Foggia, Foggia 71122, Italy.
Michał DobrakowskiDepartment of Biochemistry, Medical University of Silesia in Katowice, Zabrze 41-808, Poland.
Aleksandra KasperczykDepartment of Biochemistry, Medical University of Silesia in Katowice, Zabrze 41-808, Poland.
Sławomir KasperczykDepartment of Biochemistry, Medical University of Silesia in Katowice, Zabrze 41-808, Poland.
Palok AichSchool of Biological Sciences, National Institute of Science Education and Research, Khurdha 752050, India.
Shivaram P SinghDepartment of Gastroenterology, SCB Medical College, Cuttack 753007, India.
Gaetano ServiddioDepartment of Medical and Surgical Sciences, University of Foggia, Foggia 71122, Italy.
Gianluigi VendemialeDepartment of Medical and Surgical Sciences, University of Foggia, Foggia 71122, Italy.
University of Foggia · ITSriram Chandra Bhanja Medical College Hospital · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSodium glucose cotransporter-2 inhibitors (SGLT2-I) are the most recently approved drugs for type 2 diabetes (T2D). Recent clinical trials of these compounds reported beneficial cardiovascular (CV) and renal outcomes. A major cause of vascular dysfunction and CV disease in diabetes is hyperglycemia associated with inflammation and oxidative stress. Pre-clinical studies demonstrated that SGLT2-I reduce glucotoxicity and promote anti-inflammatory effects by lowering oxidative stress.

aimTo investigate the effects of SGLT2-I on markers of oxidative stress, inflammation, liver steatosis, and fibrosis in patients of T2D with non-alcoholic fatty liver disease (NAFLD).

methodsWe referred fifty-two consecutive outpatients treated with metformin monotherapy and exhibiting poor glycemic control to our centre. We introduced the outpatients to an SGLT2-I (dapagliflozin, empagliflozin, or canagliflozin;

resultsAdd-on therapy resulted in improved glycemic control and reduced fasting blood glucose in both groups. Of note, following treatment for six months, a reduction of FLI and APRI, as well as of the FibroScan result, was reported in patients treated with SGLT2-I, but not in the OTHER group; furthermore, in the SGLT2-I group, we reported lower circulating levels of interleukin (IL)-1β, IL-6, tumor necrosis factor, vascular endothelial growth factor, and monocyte chemoattractant protein-1, and higher levels of IL-4 and IL-10. We did not observe any modification in circulating interleukins in the OTHER group. Finally, serum HNE- and MDA-protein adducts decreased significantly in SGLT2-I rather than OTHER patients and correlated with liver steatosis and fibrosis scores.

conclusionThe present data indicate that treatment with SGLT2-I in patients with T2D and NAFLD is associated with improvement of liver steatosis and fibrosis markers and circulating pro-inflammatory and redox status, more than optimizing glycemic control.

Indexed as

Diabetes Mellitus, Type 2HepatitisNon-alcoholic Fatty Liver DiseaseSodium-Glucose Transporter 2 InhibitorsHumansHypoglycemic AgentsInflammationLiver CirrhosisOxidation-ReductionVascular Endothelial Growth Factor AHypoglycemic AgentsSodium-Glucose Transporter 2 InhibitorsVascular Endothelial Growth Factor AInflammationLiver fibrosisNon-alcoholic fatty liver diseaseOxidative stressSodium glucose cotransporter-2 inhibitorsType 2 diabetes

Identifiers

PMID36051336
PMCPMC9331534
OpenAlexW4284703609

What Socratic holds

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LicenceCC BY-NC
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 Socratic graph.