Evidence map›Paper›PMID 30290061›Full record

ArticleJournal of diabetes investigation2019

Early administration of dapagliflozin preserves pancreatic β-cell mass through a legacy effect in a mouse model of type 2 diabetes.

Ayumi Kanno, Shun-Ichiro Asahara, Mao Kawamura, Ayuko Furubayashi, Shoko Tsuchiya, Emi Suzuki, Tomoko Takai, Maki Koyanagi-Kimura, Tomokazu Matsuda, Yuko Okada and 2 more

Abstract read
In one paragraph

Article in Journal of diabetes investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–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

15 citing papers in PubMed.

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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

12 authors.

Ayumi KannoDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Shun-Ichiro AsaharaDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.ORCID http://orcid.org/0000-0001-6661-9402
Mao KawamuraDivision of Metabolism and Disease, Department of Biophysics, Kobe University Graduate School of Health Sciences, Kobe, Japan.
Ayuko FurubayashiDivision of Metabolism and Disease, Department of Biophysics, Kobe University Graduate School of Health Sciences, Kobe, Japan.
Shoko TsuchiyaDivision of Metabolism and Disease, Department of Biophysics, Kobe University Graduate School of Health Sciences, Kobe, Japan.
Emi SuzukiDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Tomoko TakaiDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Maki Koyanagi-KimuraDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Tomokazu MatsudaDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Yuko OkadaDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.ORCID http://orcid.org/0000-0001-6964-5147
Wataru OgawaDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.ORCID http://orcid.org/0000-0002-0432-4366
Yoshiaki KidoDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.ORCID http://orcid.org/0000-0003-2433-5799

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AIMS/

introductionThe preservation of pancreatic β-cell mass is an essential factor in the onset and development of type 2 diabetes mellitus. Recently, sodium-glucose cotransporter 2 inhibitors have been launched as antihyperglycemic agents, and their organ-protective effects are attracting attention. They are also reported to have favorable effects on the preservation of pancreatic β-cell mass, but the appropriate timing for the administration of sodium-glucose cotransporter 2 inhibitors is obscure. MATERIALS AND

methodsIn the present study, we administered a sodium-glucose cotransporter 2 inhibitor, dapagliflozin, to an animal model of type 2 diabetes mellitus, db/db mice, and investigated the adequate timing and duration for its administration. We also carried out microarray analysis using pancreatic islets from db/db mice.

resultsWe found that dapagliflozin preserved pancreatic β-cell mass depending on the duration of administration and markedly improved blood glucose levels. If the duration was the same, the earlier administration of dapagliflozin was more effective in preserving pancreatic β-cell mass, increasing serum insulin levels and improving blood glucose levels. From microarray analysis, we discovered that the expression of Agr2, Tff2 and Gkn3 was significantly upregulated after the early administration of dapagliflozin. This upregulated gene expression might provide a legacy effect for the preservation of pancreatic β-cell mass.

conclusionsWe expect that the early administration of dapagliflozin would provide a long-lasting effect in preserving pancreatic β-cell mass.

Indexed as

Disease Models, AnimalAnimalsBenzhydryl CompoundsBiomarkersBlood GlucoseDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2GlucosidesInsulinInsulin-Secreting CellsMaleMiceSodium-Glucose Transporter 2 InhibitorsBenzhydryl CompoundsBiomarkersBlood GlucosedapagliflozinGlucosidesInsulinSodium-Glucose Transporter 2 InhibitorsPancreatic β-cellSodium-glucose cotransporter 2Type 2 diabetes mellitus

Identifiers

PMID30290061
PMCPMC6497604

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Registered trials

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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.