Evidence map›Paper›PMID 25637831›Full record

ReviewMolecular aspects of medicine2015

Pulsatile insulin secretion, impaired glucose tolerance and type 2 diabetes.

Leslie S Satin, Peter C Butler, Joon Ha, Arthur S Sherman

Open access · greenAbstract readReview
In one paragraph

Review in Molecular aspects of medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed
15.9field-weighted citation impact, top 1% 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

124 citing papers in PubMed, 230 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Are physiological oscillations physiological?The Journal of physiology · 2026
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Glycolytic activation of β-cell NaMolecular metabolism · 2026
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

64 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

4 authors at 4 institutions in 1 country.

Leslie S SatinDepartment of Pharmacology, Brehm Diabetes Research Center, University of Michigan Medical School, Ann Arbor, MI 48105, USA. Electronic address: lsatin@umich.edu.
Peter C ButlerDepartment of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095-7073, USA.
Joon HaLaboratory of Biological Modeling, National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Arthur S ShermanLaboratory of Biological Modeling, National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
National Institute of Diabetes and Digestive and Kidney Diseases · USNational Institutes of Health · USUniversity of California, Los Angeles · USUniversity of Michigan–Ann Arbor · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
METABOLICALLY-COUPLED ION CHANNEL INTERACTIONS IN ISLETSR01DK046409 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI SATIN, LESLIE S. · 1994 to 2023
$9.1M
Role of IAPP in Islet Dysfunction in DiabetesR01DK059579 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI BUTLER, PETER CAWOOD · 2001 to 2019
$7.5M
Stimulus secretion coupling in pancreatic beta-cellsZIADK013027 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI SHERMAN, ARTHUR · 2009 to 2025
$3.6M
Intramural NIH HHSNIDDK NIH HHS P30 DK020572NIDDK NIH HHS R01 DK046409NIDDK NIH HHS R01 DK059579NIDDK NIH HHS R01 DK46409
6 · The paper itself

Abstract

Type 2 diabetes (T2DM) results when increases in beta cell function and/or mass cannot compensate for rising insulin resistance. Numerous studies have documented the longitudinal changes in metabolism that occur during the development of glucose intolerance and lead to T2DM. However, the role of changes in insulin secretion, both amount and temporal pattern, has been understudied. Most of the insulin secreted from pancreatic beta cells of the pancreas is released in a pulsatile pattern, which is disrupted in T2DM. Here we review the evidence that changes in beta cell pulsatility occur during the progression from glucose intolerance to T2DM in humans, and contribute significantly to the etiology of the disease. We review the evidence that insulin pulsatility improves the efficacy of secreted insulin on its targets, particularly hepatic glucose production, but also examine evidence that pulsatility alters or is altered by changes in peripheral glucose uptake. Finally, we summarize our current understanding of the biophysical mechanisms responsible for oscillatory insulin secretion. Understanding how insulin pulsatility contributes to normal glucose homeostasis and is altered in metabolic disease states may help improve the treatment of T2DM.

Indexed as

Insulin ResistanceAnimalsDiabetes Mellitus, Type 2FastingGlucoseHumansInsulinInsulin-Secreting CellsInsulin SecretionGlucoseInsulinDiabetesInsulin pulsatilityInsulin resistanceIsletsOscillations

Identifiers

PMID25637831
PMCPMC4696552
OpenAlexW2147387884

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.