Evidence map›Paper›PMID 37871012›Full record

ArticleDiabetes2024

Single-Cell Transcriptome Profiling of Pancreatic Islets From Early Diabetic Mice Identifies Anxa10 for Ca2+ Allostasis Toward β-Cell Failure.

Kaori Motomura, Takashi Matsuzaka, Shigeyuki Shichino, Tatsuro Ogawa, Hao Pan, Takuya Nakajima, Yasuhito Asano, Toshitsugu Okayama, Tomoyo Takeuchi, Hiroshi Ohno and 13 more

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

13 citing papers in PubMed, 11 citations in OpenAlex.

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  13. CaFrontiers in endocrinology · 2024
    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

23 authors at 8 institutions in 2 countries.

Kaori MotomuraDepartment of Endocrinology and Metabolism, Institute of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan.
Takashi MatsuzakaDepartment of Endocrinology and Metabolism, Institute of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan.
Shigeyuki ShichinoDivision of Molecular Regulation of Inflammatory and Immune Diseases, Research Institute of Biomedical Sciences, Tokyo University of Science, Noda, Japan.
Tatsuro OgawaDivision of Molecular Regulation of Inflammatory and Immune Diseases, Research Institute of Biomedical Sciences, Tokyo University of Science, Noda, Japan.
Hao PanDepartment of Bio-Science, Nagahama Institute of BioScience and Technology, Nagahama, Shiga, Japan.
Takuya NakajimaDivision of Molecular Regulation of Inflammatory and Immune Diseases, Research Institute of Biomedical Sciences, Tokyo University of Science, Noda, Japan.
Yasuhito AsanoFaculty of Information Networking for Innovation and Design, Toyo University, Tokyo, Japan.
Toshitsugu OkayamaCenter for Information Biology, National Institute of Genetics, Mishima, Japan.
Tomoyo TakeuchiTsukuba Human Tissue Biobank Center, University of Tsukuba Hospital, Ibaraki, Japan.
Hiroshi OhnoDepartment of Endocrinology and Metabolism, Institute of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan.
Song-Iee HanDepartment of Endocrinology and Metabolism, Institute of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan.
Takafumi MiyamotoDepartment of Endocrinology and Metabolism, Institute of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan.
Yoshinori TakeuchiDepartment of Endocrinology and Metabolism, Institute of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan.
Motohiro SekiyaDepartment of Endocrinology and Metabolism, Institute of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan.
Hirohito SoneDepartment of Hematology, Endocrinology and Metabolism, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.ORCID 0000-0003-1263-2817
Naoya YahagiDepartment of Endocrinology and Metabolism, Institute of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan.
Yoshimi NakagawaDivision of Complex Biosystem Research, Department of Research and Development, Institute of Natural Medicine, University of Toyama, Toyama, Japan.
Tatsuya OdaDepartment of Gastrointestinal and Hepatobiliary Pancreatic Surgery, Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan.
Satoshi UehaDivision of Molecular Regulation of Inflammatory and Immune Diseases, Research Institute of Biomedical Sciences, Tokyo University of Science, Noda, Japan.
Kazuho IkeoCenter for Information Biology, National Institute of Genetics, Mishima, Japan.
Atsushi OguraDepartment of Bio-Science, Nagahama Institute of BioScience and Technology, Nagahama, Shiga, Japan.
Kouji MatsushimaDivision of Molecular Regulation of Inflammatory and Immune Diseases, Research Institute of Biomedical Sciences, Tokyo University of Science, Noda, Japan.
Hitoshi ShimanoDepartment of Endocrinology and Metabolism, Institute of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan.ORCID 0000-0002-5562-5572
University of Tsukuba · JPTokyo University of Science · JPNagahama Institute of Bio-Science and Technology · JPNational Institute of Genetics · JPNiigata University Medical and Dental Hospital · JPToyama College · JPToyo University · JPUniversity of Tsukuba Hospital · JP

Funding

Grants-in-aid for Scientific Research on Innovative Areas program (Inflammation Cellular Sociology) JP17H06391
6 · The paper itself

Abstract

Type 2 diabetes is a progressive disorder denoted by hyperglycemia and impaired insulin secretion. Although a decrease in β-cell function and mass is a well-known trigger for diabetes, the comprehensive mechanism is still unidentified. Here, we performed single-cell RNA sequencing of pancreatic islets from prediabetic and diabetic db/db mice, an animal model of type 2 diabetes. We discovered a diabetes-specific transcriptome landscape of endocrine and nonendocrine cell types with subpopulations of β- and α-cells. We recognized a new prediabetic gene, Anxa10, that was induced by and regulated Ca2+ influx from metabolic stresses. Anxa10-overexpressed β-cells displayed suppression of glucose-stimulated intracellular Ca2+ elevation and potassium-induced insulin secretion. Pseudotime analysis of β-cells predicted that this Ca2+-surge responder cluster would proceed to mitochondria dysfunction and endoplasmic reticulum stress. Other trajectories comprised dedifferentiation and transdifferentiation, emphasizing acinar-like cells in diabetic islets. Altogether, our data provide a new insight into Ca2+ allostasis and β-cell failure processes. ARTICLE HIGHLIGHTS: The transcriptome of single-islet cells from healthy, prediabetic, and diabetic mice was studied. Distinct β-cell heterogeneity and islet cell-cell network in prediabetes and diabetes were found. A new prediabetic β-cell marker, Anxa10, regulates intracellular Ca2+ and insulin secretion. Diabetes triggers β-cell to acinar cell transdifferentiation.

Indexed as

AllostasisDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Insulin-Secreting CellsIslets of LangerhansPrediabetic StateAnimalsAnnexinsCalciumGene Expression ProfilingInsulinMiceMice, Inbred StrainsAnnexinsAnxa10 protein, mouseCalciumInsulin

Identifiers

PMID37871012
PMCPMC10784657
OpenAlexW4387873388

What OpenQuestion holds

Textmetadata
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.