Evidence map›Paper›PMID 35185578›Full record

ArticleFrontiers in pharmacology2022

The Treatment With the SGLT2 Inhibitor Empagliflozin Modifies the Hepatic Metabolome of Male Zucker Diabetic Fatty Rats Towards a Protective Profile.

Alana Aragón-Herrera, Manuel Otero-Santiago, Laura Anido-Varela, Sandra Moraña-Fernández, Manuel Campos-Toimil, Tomás García-Caballero, Luis Barral, Estefanía Tarazón, Esther Roselló-Lletí, Manuel Portolés and 6 more

Abstract read
In one paragraph

Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

8 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. 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

16 authors.

Alana Aragón-HerreraCellular and Molecular Cardiology Research Unit, Institute of Biomedical Research and Xerencia de Xestión Integrada de Santiago (XXIS/SERGAS), Santiago de Compostela, Spain.
Manuel Otero-SantiagoCellular and Molecular Cardiology Research Unit, Institute of Biomedical Research and Xerencia de Xestión Integrada de Santiago (XXIS/SERGAS), Santiago de Compostela, Spain.
Laura Anido-VarelaCellular and Molecular Cardiology Research Unit, Institute of Biomedical Research and Xerencia de Xestión Integrada de Santiago (XXIS/SERGAS), Santiago de Compostela, Spain.
Sandra Moraña-FernándezCellular and Molecular Cardiology Research Unit, Institute of Biomedical Research and Xerencia de Xestión Integrada de Santiago (XXIS/SERGAS), Santiago de Compostela, Spain.
Manuel Campos-ToimilGroup of Pharmacology of Chronic Diseases (CD Pharma), Department of Pharmacology, Pharmacy and Pharmaceutical Technology, University of Santiago de Compostela, Santiago de Compostela, Spain.
Tomás García-CaballeroDepartment of Morphological Sciences, University of Santiago de Compostela and Xerencia de Xestión Integrada de Santiago (XXIS/SERGAS), Santiago de Compostela, Spain.
Luis BarralGroup of Polymers, Department of Physics and Earth Sciences, University of La Coruña, La Coruña, Spain.
Estefanía TarazónCentro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Institute of Health Carlos III, Madrid, Spain.
Esther Roselló-LletíCentro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Institute of Health Carlos III, Madrid, Spain.
Manuel PortolésCentro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Institute of Health Carlos III, Madrid, Spain.
Oreste GualilloLaboratory of Neuroendocrine Interactions in Rheumatology and Inflammatory Diseases, Institute of Biomedical Research and Xerencia de Xestión Integrada de Santiago (XXIS/SERGAS), Santiago de Compostela, Spain.
Isabel MoscosoCardiology Group, Center for Research in Molecular Medicine and Chronic Diseases (CIMUS) and Institute of Biomedical Research of Santiago de Compostela (IDIS-SERGAS), Universidade de Santiago de Compostela, Santiago de Compostela, Spain.
Ricardo LageCardiology Group, Center for Research in Molecular Medicine and Chronic Diseases (CIMUS) and Institute of Biomedical Research of Santiago de Compostela (IDIS-SERGAS), Universidade de Santiago de Compostela, Santiago de Compostela, Spain.
José Ramón González-JuanateyCellular and Molecular Cardiology Research Unit, Institute of Biomedical Research and Xerencia de Xestión Integrada de Santiago (XXIS/SERGAS), Santiago de Compostela, Spain.
Sandra Feijóo-BandínCellular and Molecular Cardiology Research Unit, Institute of Biomedical Research and Xerencia de Xestión Integrada de Santiago (XXIS/SERGAS), Santiago de Compostela, Spain.
Francisca LagoCellular and Molecular Cardiology Research Unit, Institute of Biomedical Research and Xerencia de Xestión Integrada de Santiago (XXIS/SERGAS), Santiago de Compostela, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The EMPA-REG OUTCOME (Empagliflozin, Cardiovascular Outcome Event Trial in patients with Type 2 Diabetes Mellitus (T2DM)) trial evidenced the potential of sodium-glucose cotransporter 2 (SGLT2) inhibitors for the treatment of patients with diabetes and cardiovascular disease. Recent evidences have shown the benefits of the SGLT2 inhibitor empagliflozin on improving liver steatosis and fibrosis in patients with T2DM. Metabolomic studies have been shown to be very useful to improve the understanding of liver pathophysiology during the development and progression of metabolic hepatic diseases, and because the effects of empagliflozin and of other SGLT2 inhibitors on the complete metabolic profile of the liver has never been analysed before, we decided to study the impact on the liver of male Zucker diabetic fatty (ZDF) rats of a treatment for 6 weeks with empagliflozin using an untargeted metabolomics approach, with the purpose to help to clarify the benefits of the use of empagliflozin at hepatic level. We found that empagliflozin is able to change the hepatic lipidome towards a protective profile, through an increase of monounsaturated and polyunsaturated glycerides, phosphatidylcholines, phosphatidylethanolamines, lysophosphatidylinositols and lysophosphatidylcholines. Empagliflozin also induces a decrease in the levels of the markers of inflammation IL-6, chemerin and chemerin receptor in the liver. Our results provide new evidences regarding the molecular pathways through which empagliflozin could exert hepatoprotector beneficial effects in T2DM.

Indexed as

diabetesempagliflozininflammationlivermetabolome

Identifiers

PMID35185578
PMCPMC8847595

What OpenQuestion holds

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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.