Evidence map›Paper›PMID 23969997›Full record

ReviewExperimental & molecular medicine2013

Signaling mechanisms of glucose-induced F-actin remodeling in pancreatic islet β cells.

Michael A Kalwat, Debbie C Thurmond

Open access · goldAbstract readReview
In one paragraph

Review in Experimental & molecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
9.9field-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

89 citing papers in PubMed, 158 citations in OpenAlex.

  1. Article
  2. Activation of GScience advances · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Glycolytic activation of β-cell NaMolecular metabolism · 2026
    Article
  7. Article
  8. Roles of molecular motors in insulin-secreting beta cells.Current opinion in cell biology · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Investigating the Mechanisms ofFood science & nutrition · 2025
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Mechanisms of spinophilin-dependent pancreas dysregulation in obesity.American journal of physiology. Endocrinology and metabolism · 2024
    Article
  20. Article

29 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

2 authors at 2 institutions in 1 country.

Michael A KalwatDepartment of Pharmacology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Debbie C Thurmond
Indiana University School of MedicineThe University of Texas Southwestern Medical Center · US

Funding

Regulation of Glucose Homeostasis by Munc18 ProteinsR01DK067912 · NIDDK · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI THURMOND, DEBBIE C · 2004 to 2023
$6.5M
Cdc42-regulated insulin granule exocytosisR01DK076614 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI THURMOND, DEBBIE C · 2008 to 2012
$1.6M
NIDDK NIH HHS DK067912NIDDK NIH HHS DK076614NIDDK NIH HHS R01 DK067912NIDDK NIH HHS R01 DK076614
6 · The paper itself

Abstract

The maintenance of whole-body glucose homeostasis is critical for survival, and is controlled by the coordination of multiple organs and endocrine systems. Pancreatic islet β cells secrete insulin in response to nutrient stimuli, and insulin then travels through the circulation promoting glucose uptake into insulin-responsive tissues such as liver, skeletal muscle and adipose. Many of the genes identified in human genome-wide association studies of diabetic individuals are directly associated with β cell survival and function, giving credence to the idea that β-cell dysfunction is central to the development of type 2 diabetes. As such, investigations into the mechanisms by which β cells sense glucose and secrete insulin in a regulated manner are a major focus of current diabetes research. In particular, recent discoveries of the detailed role and requirements for reorganization/remodeling of filamentous actin (F-actin) in the regulation of insulin release from the β cell have appeared at the forefront of islet function research, having lapsed in prior years due to technical limitations. Recent advances in live-cell imaging and specialized reagents have revealed localized F-actin remodeling to be a requisite for the normal biphasic pattern of nutrient-stimulated insulin secretion. This review will provide an historical look at the emergent focus on the role of the actin cytoskeleton and its regulation of insulin secretion, leading up to the cutting-edge research in progress in the field today.

Indexed as

ActinsAnimalsExocytosisGlucoseHumansInsulinInsulin-Secreting CellsSignal TransductionActinsGlucoseInsulin

Identifiers

PMID23969997
PMCPMC3789261
OpenAlexW2002800164

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.