Evidence map›Paper›PMID 35115614›Full record

Trial reportScientific reports2022

The sodium-glucose cotransporter 2 inhibitor ipragliflozin improves liver function and insulin resistance in Japanese patients with type 2 diabetes.

Tsuyoshi Okura, Yohei Fujioka, Risa Nakamura, Sonoko Kitao, Yuichi Ito, Mari Anno, Kazuhisa Matsumoto, Kyoko Shoji, Kazuhiko Matsuzawa, Shoichiro Izawa and 6 more

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Review
  5. Article
  6. Article
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 at 1 institution in 1 country.

Tsuyoshi OkuraDivision of Cardiovascular Medicine, Endocrinology and Metabolism, Tottori University Faculty of Medicine, 36-1 Nishi-Cho, Yonago, Tottori, 683-8504, Japan. ohkura@tottori-u.ac.jp.ORCID 0000-0003-3713-6617
Yohei FujiokaDivision of Cardiovascular Medicine, Endocrinology and Metabolism, Tottori University Faculty of Medicine, 36-1 Nishi-Cho, Yonago, Tottori, 683-8504, Japan.
Risa NakamuraDivision of Cardiovascular Medicine, Endocrinology and Metabolism, Tottori University Faculty of Medicine, 36-1 Nishi-Cho, Yonago, Tottori, 683-8504, Japan.
Sonoko KitaoDivision of Cardiovascular Medicine, Endocrinology and Metabolism, Tottori University Faculty of Medicine, 36-1 Nishi-Cho, Yonago, Tottori, 683-8504, Japan.
Yuichi ItoDivision of Cardiovascular Medicine, Endocrinology and Metabolism, Tottori University Faculty of Medicine, 36-1 Nishi-Cho, Yonago, Tottori, 683-8504, Japan.
Mari AnnoDivision of Cardiovascular Medicine, Endocrinology and Metabolism, Tottori University Faculty of Medicine, 36-1 Nishi-Cho, Yonago, Tottori, 683-8504, Japan.
Kazuhisa MatsumotoDivision of Cardiovascular Medicine, Endocrinology and Metabolism, Tottori University Faculty of Medicine, 36-1 Nishi-Cho, Yonago, Tottori, 683-8504, Japan.
Kyoko ShojiDivision of Cardiovascular Medicine, Endocrinology and Metabolism, Tottori University Faculty of Medicine, 36-1 Nishi-Cho, Yonago, Tottori, 683-8504, Japan.
Kazuhiko MatsuzawaDivision of Cardiovascular Medicine, Endocrinology and Metabolism, Tottori University Faculty of Medicine, 36-1 Nishi-Cho, Yonago, Tottori, 683-8504, Japan.
Shoichiro IzawaDivision of Cardiovascular Medicine, Endocrinology and Metabolism, Tottori University Faculty of Medicine, 36-1 Nishi-Cho, Yonago, Tottori, 683-8504, Japan.
Hiroko OkuraDivision of Cardiovascular Medicine, Endocrinology and Metabolism, Tottori University Faculty of Medicine, 36-1 Nishi-Cho, Yonago, Tottori, 683-8504, Japan.
Etsuko UetaSchool of Health Science, Tottori University Faculty of Medicine, Yonago, Japan.
Masahiko KatoSchool of Health Science, Tottori University Faculty of Medicine, Yonago, Japan.
Takeshi ImamuraDivision of Molecular Pharmacology, Tottori University Faculty of Medicine, Yonago, Japan.
Shin-Ichi TaniguchiDepartment of Regional Medicine, Tottori University Faculty of Medicine, Yonago, Japan.
Kazuhiro YamamotoDivision of Cardiovascular Medicine, Endocrinology and Metabolism, Tottori University Faculty of Medicine, 36-1 Nishi-Cho, Yonago, Tottori, 683-8504, Japan.
Tottori University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sodium-glucose cotransporter 2 inhibitor (SGLT2i) treatment is a therapeutic approach for type 2 diabetes mellitus (T2DM). Some reports have shown that SGLT2i treatment improves insulin resistance; however, few studies have evaluated insulin resistance by the glucose clamp method. Hepatic insulin clearance (HIC) is a new pathophysiological mechanism of T2DM. The effect of SGLT2i treatment on hepatic insulin clearance and insulin resistance is not well known. We investigated the effect of SGLT2i treatment on insulin resistance, insulin secretion, incretin levels, body composition, and hepatic insulin clearance. We conducted a meal tolerance test (MTT) and a hyperinsulinemic-euglycemic clamp test in 9 T2DM patients. Ipragliflozin (50 mg/day) was administered, and the MTT and clamp test were performed after 4 months. We calculated HIC as the postprandial C-peptide AUC-to-insulin AUC ratio. We also measured GLP-1, GIP, and glucagon levels during the MTT. Body weight and HbA1c were decreased, although not significantly, after 4 months of treatment. Postprandial glucose, fasting insulin and postprandial insulin were significantly decreased. Insulin resistance with the glucose clamp was not changed, but the HOMA-IR and insulin sensitivity indices were significantly improved. Incretin and glucagon levels were not changed. Hepatic insulin clearance was significantly increased, but whole-body insulin clearance was not changed. The FIB-4 index and fatty liver index were significantly reduced. The HOMA-beta and insulinogenic indices were not changed, but the C-peptide index was significantly increased. Although the number of patients was small, these results suggested that SGLT2i treatment improved liver function, decreased hepatic insulin resistance, and increased hepatic insulin clearance, despite the small weight reduction.

Indexed as

Insulin ResistanceBiomarkersBlood GlucoseDiabetes Mellitus, Type 2FemaleGastric Inhibitory PolypeptideGlucagonGlucagon-Like Peptide 1GlucosidesHumansInsulinJapanLiverMaleMiddle AgedSodium-Glucose Transporter 2 InhibitorsBiomarkersBlood GlucoseGastric Inhibitory PolypeptideGlucagonGlucagon-Like Peptide 1GlucosidesInsulinipragliflozinSodium-Glucose Transporter 2 InhibitorsThiophenes

Identifiers

PMID35115614
PMCPMC8814145
OpenAlexW4210467374

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.