Evidence map›Paper›PMID 32821334›Full record

ArticleWorld journal of hepatology2020

Ipragliflozin-induced improvement of liver steatosis in obese mice may involve sirtuin signaling.

Takayoshi Suga, Ken Sato, Tatsuya Ohyama, Sho Matsui, Takeshi Kobayashi, Hiroki Tojima, Norio Horiguchi, Yuichi Yamazaki, Satoru Kakizaki, Ayaka Nishikido and 4 more

Open access · diamondAbstract read
In one paragraph

Article in World journal of hepatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Exploring Promising Therapies for Non-Alcoholic Fatty Liver Disease: A ClinicalTrials.gov Analysis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Review
  8. Article
  9. Review
  10. 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

14 authors at 1 institution in 1 country.

Takayoshi SugaDepartment of Gastroenterology and Hepatology, Gunma University Graduate School of Medicine, Maebashi 371-8511, Gunma, Japan.
Ken SatoDepartment of Gastroenterology and Hepatology, Gunma University Graduate School of Medicine, Maebashi 371-8511, Gunma, Japan. satoken@gunma-u.ac.jp.
Tatsuya OhyamaDepartment of Gastroenterology and Hepatology, Gunma University Graduate School of Medicine, Maebashi 371-8511, Gunma, Japan.
Sho MatsuiMetabolic Signal Research Center, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi 371-8512, Gunma, Japan.
Takeshi KobayashiDepartment of Gastroenterology and Hepatology, Gunma University Graduate School of Medicine, Maebashi 371-8511, Gunma, Japan.
Hiroki TojimaDepartment of Gastroenterology and Hepatology, Gunma University Graduate School of Medicine, Maebashi 371-8511, Gunma, Japan.
Norio HoriguchiDepartment of Gastroenterology and Hepatology, Gunma University Graduate School of Medicine, Maebashi 371-8511, Gunma, Japan.
Yuichi YamazakiDepartment of Gastroenterology and Hepatology, Gunma University Graduate School of Medicine, Maebashi 371-8511, Gunma, Japan.
Satoru KakizakiDepartment of Gastroenterology and Hepatology, Gunma University Graduate School of Medicine, Maebashi 371-8511, Gunma, Japan.
Ayaka NishikidoDepartment of Medicine and Molecular Science, Gunma Graduate School of Medicine, Maebashi 371-8511, Gunma, Japan.
Takashi OkamuraDepartment of Medicine and Molecular Science, Gunma Graduate School of Medicine, Maebashi 371-8511, Gunma, Japan.
Masanobu YamadaDepartment of Medicine and Molecular Science, Gunma Graduate School of Medicine, Maebashi 371-8511, Gunma, Japan.
Tadahiro KitamuraMetabolic Signal Research Center, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi 371-8512, Gunma, Japan.
Toshio UraokaDepartment of Gastroenterology and Hepatology, Gunma University Graduate School of Medicine, Maebashi 371-8511, Gunma, Japan.
Gunma University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSodium glucose cotransporter 2 (SGLT2) inhibitors are newly developed oral antidiabetic drugs. SGLT2 is primarily expressed in the kidneys and reabsorbs approximately 90% of the glucose filtered by the renal glomeruli. SGLT2 inhibitors lower glucose levels independently of insulin action by facilitating urinary glucose excretion. The SGLT2 inhibitor ipragliflozin has reportedly improved liver steatosis in animal models and clinical studies. However, the mechanisms by which SGLT2 inhibitors improve liver steatosis are not fully understood.

aimTo investigate the ameliorative effects of ipragliflozin on liver steatosis and the mechanisms of these effects in obese mice.

methodsWe analyzed 8-wk-old male obese (

resultsHepatic lipid accumulation was significantly ameliorated in

conclusionOur study suggests that the liver steatosis-ameliorating effects of ipragliflozin in

Indexed as

Fibroblast growth factor-21Nonalcoholic fatty liver diseasePeroxisome proliferator-activated receptor αPeroxisome proliferator-activated receptor γ coactivator 1αSelective sodium glucose cotransporter 2Sirtuin 1

Identifiers

PMID32821334
PMCPMC7407917
OpenAlexW3044739183

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.