Evidence map›Paper›PMID 34298949›Full record

ArticleInternational journal of molecular sciences2021

Ipragliflozin Ameliorates Diabetic Nephropathy Associated with Perirenal Adipose Expansion in Mice.

Hideyuki Okuma, Kentaro Mori, Suguru Nakamura, Tetsuo Sekine, Yoshihiro Ogawa, Kyoichiro Tsuchiya

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Anti-Inflammatory Effects of SGLT2 Inhibitors: Focus on Macrophages.International journal of molecular sciences · 2025
    Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
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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

6 authors at 3 institutions in 1 country.

Hideyuki OkumaInterdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo 4093898, Japan.
Kentaro MoriInterdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo 4093898, Japan.
Suguru NakamuraInterdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo 4093898, Japan.
Tetsuo SekineInterdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo 4093898, Japan.
Yoshihiro OgawaDepartment of Medicine and Bioregulatory Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka 8168580, Japan.ORCID 0000-0002-0834-2836
Kyoichiro TsuchiyaDepartment of Diabetes and Endocrinology, University of Yamanashi Hospital, Chuo 4093898, Japan.
University of Yamanashi · JPKyushu University · JPUniversity of Yamanashi Hospital · JP

Funding

Japan Society for the Promotion of Science 20K08883
6 · The paper itself

Abstract

Sodium glucose cotransporter-2 (SGLT2) inhibitors inhibit the development of diabetic nephropathy (DN). We determined whether changes in perirenal fat (PRAT) by a SGLT2 inhibitor ipragliflozin (Ipra) contribute to the suppression of DN development. High-fat diet (HFD)-fed mice were used as a DN model and were treated with or without Ipra for 6 weeks. Ipra treatment reduced urinary albumin excretion (UAE) and glomerular hypertrophy in HFD-fed mice. In the PRAT of Ipra-treated mice, adipocyte size was increased, and inflammation, fibrosis, and adipocyte death were suppressed. In conditioned medium made from PRAT (PRAT-CM) of Ipra-treated mice, the concentration of leptin was significantly lower than PRAT-CM of mice without Ipra treatment. Serum leptin concentration in renal vein positively correlated with UAE. PRAT-CM from HFD-fed mice showed greater cell proliferation signaling in mouse glomerular endothelial cells (GECs) than PRAT-CM from standard diet-fed mice via p38MAPK and leptin-dependent pathways, whose effects were significantly attenuated in PRAT-CM from Ipra-treated mice. These findings suggest that Ipra-induced PRAT expansion may play an important role in the improvement of DN in HFD-fed mice. In vitro experiments suggest that reduced PRAT-derived leptin by Ipra could inhibit GECs proliferation, possibly contributing to the suppression of DN development.

Indexed as

Diabetes Mellitus, ExperimentalDiabetic NephropathiesAdipose TissueAnimalsGlucosidesKidney GlomerulusMaleMiceSodium-Glucose Transporter 2 InhibitorsThiophenesGlucosidesipragliflozinSodium-Glucose Transporter 2 InhibitorsThiophenesadipose tissuediabetic nephropathySGLT2 inhibitors

Identifiers

PMID34298949
PMCPMC8304702
OpenAlexW3182847562

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.