Evidence map›Paper›PMID 19187772›Full record

ArticleCell metabolism2009

Secondary consequences of beta cell inexcitability: identification and prevention in a murine model of K(ATP)-induced neonatal diabetes mellitus.

Maria Sara Remedi, Harley T Kurata, Alexis Scott, F Thomas Wunderlich, Eva Rother, Andre Kleinridders, Ailing Tong, Jens C Brüning, Joseph C Koster, Colin G Nichols

Open access · bronzeAbstract read
In one paragraph

Article in Cell metabolism, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
7.1field-weighted citation impact, top 3% 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

66 citing papers in PubMed, 98 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Personalized Therapeutics for KAnnual review of pharmacology and toxicology · 2023
    Review
  9. Article
  10. Dynamic changes in β-cell [CaMolecular metabolism · 2022
    Article
  11. Article
  12. Article
  13. Cognitive deficits and impaired hippocampal long-term potentiation in KProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  14. Structure based analysis of KScientific reports · 2021
    Article
  15. PDX1Nature communications · 2021
    Article
  16. New insights into KNature reviews. Endocrinology · 2020
    Review
  17. Primary cilia control glucose homeostasis via islet paracrine interactions.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  18. Article
  19. Article
  20. Article

6 more citing papers are in PubMed but not listed here.

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

10 authors at 3 institutions in 2 countries.

Maria Sara RemediDepartment of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Harley T Kurata
Alexis Scott
F Thomas Wunderlich
Eva Rother
Andre Kleinridders
Ailing Tong
Jens C Brüning
Joseph C Koster
Colin G Nichols
Washington University in St. Louis · USCologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEUniversity of Cologne · DE

Funding

WU P&FP30DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI Jennifer Lynn Powers Carson · 2013 to 2026
$27.1M
TRANSGENICS COREP60DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI SCHAFFER, JEAN E. · 1986 to 2012
$25.2M
ELECTRICAL CONTROL OF INSULIN SECRETIONR01DK069445 · NIDDK · WASHINGTON UNIVERSITY · PI NICHOLS, COLIN G · 2005 to 2013
$2.9M
NIDDK NIH HHS DK20579NIDDK NIH HHS DK69445NIDDK NIH HHS P30 DK020579NIDDK NIH HHS P60 DK020579NIDDK NIH HHS R01 DK069445
6 · The paper itself

Abstract

ATP-insensitive K(ATP) channel mutations cause neonatal diabetes mellitus (NDM). To explore the mechanistic etiology, we generated transgenic mice carrying an ATP-insensitive mutant K(ATP) channel subunit. Constitutive expression in pancreatic beta cells caused neonatal hyperglycemia and progression to severe diabetes and growth retardation, with loss of islet insulin content and beta cell architecture. Tamoxifen-induced expression in adult beta cells led to diabetes within 2 weeks, with similar secondary consequences. Diabetes was prevented by transplantation of normal islets under the kidney capsule. Moreover, the endogenous islets maintained normal insulin content and secretion in response to sulfonylureas, but not glucose, consistent with reduced ATP sensitivity of beta cell K(ATP) channels. In NDM, transfer to sulfonylurea therapy is less effective in older patients. This may stem from poor glycemic control or lack of insulin because glibenclamide treatment prior to tamoxifen induction prevented diabetes and secondary complications in mice but failed to halt disease progression after diabetes had developed.

Indexed as

Adenosine TriphosphateAnimalsAnimals, NewbornBlood GlucoseDiabetes Mellitus, ExperimentalGlyburideInsulinInsulin-Secreting CellsInsulin SecretionKATP ChannelsMiceMice, TransgenicModels, AnimalSulfonylurea CompoundsTamoxifenAdenosine TriphosphateBlood GlucoseGlyburideInsulinKATP ChannelsSulfonylurea CompoundsTamoxifen

Identifiers

PMID19187772
PMCPMC4793729
OpenAlexW2010209728

What OpenQuestion holds

Textmetadata
LicenceTDM
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.