Evidence map›Paper›PMID 15630453›Full record

ArticleThe Journal of clinical investigation2005

PKClambda regulates glucose-induced insulin secretion through modulation of gene expression in pancreatic beta cells.

Naoko Hashimoto, Yoshiaki Kido, Tohru Uchida, Tomokazu Matsuda, Kazuhisa Suzuki, Hiroshi Inoue, Michihiro Matsumoto, Wataru Ogawa, Sakan Maeda, Hiroaki Fujihara and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
8.5field-weighted citation impact, top 2% 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

26 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
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  10. Epidermal polarity genes in health and disease.Cold Spring Harbor perspectives in medicine · 2014
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  17. Metabolic functions of atypical protein kinase C: "good" and "bad" as defined by nutritional status.American journal of physiology. Endocrinology and metabolism · 2010
    Review
  18. Article
  19. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 6 institutions in 2 countries.

Naoko HashimotoDepartment of Clinical Molecular Medicine, Division of Diabetes and Digestive and Kidney Diseases, Kobe University Graduate School of Medicine, Kobe, Japan.
Yoshiaki Kido
Tohru Uchida
Tomokazu Matsuda
Kazuhisa Suzuki
Hiroshi Inoue
Michihiro Matsumoto
Wataru Ogawa
Sakan Maeda
Hiroaki Fujihara
Yoichi Ueta
Yasuo Uchiyama
Kazunori Akimoto
Shigeo Ohno
Tetsuo Noda
Masato Kasuga
Kidney Associates · USKobe University · JPUniversity of Occupational and Environmental Health Japan · JPJapanese Foundation For Cancer Research · JPThe University of Osaka · JPYokohama City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Altered regulation of insulin secretion by glucose is characteristic of individuals with type 2 diabetes mellitus, although the mechanisms that underlie this change remain unclear. We have now generated mice that lack the lambda isoform of PKC in pancreatic beta cells (betaPKClambda(-/-) mice) and show that these animals manifest impaired glucose tolerance and hypoinsulinemia. Furthermore, insulin secretion in response to high concentrations of glucose was impaired, whereas the basal rate of insulin release was increased, in islets isolated from betaPKClambda(-/-) mice. Neither the beta cell mass nor the islet insulin content of betaPKClambda(-/-) mice differed from that of control mice, however. The abundance of mRNAs for Glut2 and HNF3beta was reduced in islets of betaPKClambda(-/-) mice, and the expression of genes regulated by HNF3beta was also affected (that of Sur1 and Kir6.2 genes was reduced, whereas that of hexokinase 1 and hexokinase 2 genes was increased). Normalization of HNF3beta expression by infection of islets from betaPKClambda(-/-) mice with an adenoviral vector significantly reversed the defect in glucose-stimulated insulin secretion. These results indicate that PKClambda plays a prominent role in regulation of glucose-induced insulin secretion by modulating the expression of genes important for beta cell function.

Indexed as

Gene Expression RegulationAnimalsDietary FatsDNA-Binding ProteinsGene DeletionGlucoseHepatocyte Nuclear Factor 3-betaInsulinInsulin SecretionIslets of LangerhansIsoenzymesMiceMice, KnockoutMicroscopy, ElectronNuclear ProteinsProtein Kinase CDietary FatsDNA-Binding ProteinsFoxa2 protein, mouseGlucoseHepatocyte Nuclear Factor 3-betaInsulinIsoenzymesNuclear ProteinsProtein Kinase CProtein Kinase C-lambdaTranscription Factors

Identifiers

PMID15630453
PMCPMC539193
OpenAlexW2106340369

What Socratic 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 Socratic graph.