Evidence map›Paper›PMID 23211512›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2013

Neuropeptide Y and somatostatin inhibit insulin secretion through different mechanisms.

Tara A Schwetz, Alessandro Ustione, David W Piston

Abstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

21 citing papers in PubMed, 40 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Role of complexin 2 in the regulation of hormone secretion from the islet of Langerhans.American journal of physiology. Endocrinology and metabolism · 2025
    Article
  4. Review
  5. Brain-Body Communication in Glucose Metabolism.Advances in experimental medicine and biology · 2025
    Review
  6. Phylogenetic conservation of the interdependent homeostatic relationship of sleep regulation and redox metabolism.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2024
    Review
  7. Article
  8. Review
  9. Article
  10. Somatostatin analogues for the treatment of hyperinsulinaemic hypoglycaemia.Therapeutic advances in endocrinology and metabolism · 2020
    Review
  11. Review
  12. Article
  13. Article
  14. Pancreatic regulation of glucose homeostasis.Experimental & molecular medicine · 2016
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

3 authors at 2 institutions in 1 country.

Tara A SchwetzDepartment of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Alessandro Ustione
David W Piston
Vanderbilt University Medical Center · USVanderbilt University · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Ben Ho Park · 1995 to 2026
$172.8M
Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MARY Kay WASHINGTON · 2002 to 2026
$29.9M
Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI OWEN P MCGUINNESS · 2012 to 2026
$29.3M
TRANSGENIC MOUSE/ ES CELL SHARES RESOURCESP60DK020593 · NIDDK · VANDERBILT UNIVERSITY · PI ELASY, TOM A · 1986 to 2011
$28.1M
Shop Module CoreP30EY008126 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI David J. Calkins · 1989 to 2026
$19.6M
THREE-TIERED PREVENTION MODEL TO BETTER SERVE ALL STUDENP30HD015052 · NICHD · VANDERBILT UNIVERSITY · PI HARRELL, FRANK E. · 1985 to 2014
$18.6M
MULTIDISCIPLINARY TRAINING IN MOLECULAR ENDOCRINOLOGYT32DK007563 · NIDDK · VANDERBILT UNIVERSITY · PI Richard M O'Brien · 1988 to 2026
$15.9M
Vanderbilt Mouse Metabolic Physiology CenterU24DK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2001 to 2015
$14.9M
DYNAMICS OF PANCREATIC ISLET FUNCTIONR01DK053434 · NIDDK · VANDERBILT UNIVERSITY · PI PISTON, DAVID W · 1998 to 2010
$3.1M
Dopamine Action in Pancreatic Islet FunctionR01DK085064 · NIDDK · WASHINGTON UNIVERSITY · PI PISTON, DAVID W · 2010 to 2014
$1.7M
Modulation of insulin and glucagon secretion by GPCR ligandsF32DK091181 · NIDDK · VANDERBILT UNIVERSITY · PI SCHWETZ, TARA ASHLEY · 2011 to 2011
$51k
NCI NIH HHS CA-68485NEI NIH HHS EY-08126NICHD NIH HHS HD-15052NIDDK NIH HHS DK-20593NIDDK NIH HHS DK-58404NIDDK NIH HHS DK-59637NIDDK NIH HHS F32 DK-091181NIDDK NIH HHS R01 DK-053434NIDDK NIH HHS R01 DK-085064NIDDK NIH HHS R01 DK085064NIDDK NIH HHS T32 DK-007563NIDDK NIH HHS T32 DK007563
6 · The paper itself

Abstract

Pancreatic β-cells regulate glucose homeostasis by secreting insulin in response to glucose elevation and G protein-coupled receptor (GPCR) activation. Neuropeptide Y (NPY) and somatostatin (SST) attenuate insulin secretion through G(i) activation of Y(1) and SSTR(1&5) receptors, respectively. The downstream pathways altered by NPY and SST are poorly understood. Thus, we investigated these underlying mechanisms. NPY and SST increase cellular redox potential, suggesting that their inhibitory effect may not be mediated through metabolic inhibition. NPY does not affect intracellular calcium ([Ca(2+)](i)) activity upon glucose stimulation, whereas SST alters this response. G(βγ)-subunit inhibition by gallein attenuates insulin secretion but does not alter metabolism or [Ca(2+)](i). mSIRK-induced G(βγ) activation does not modulate glucose metabolism but increases [Ca(2+)](i) activity and potentiates insulin release. Cotreatment with gallein and NPY or SST reduces insulin secretion to levels similar to that of gallein alone. mSIRK and NPY cotreatment potentiates insulin secretion similarly to mSIRK alone, whereas mSIRK and SST treatment decreases insulin release. The data support a model where SST attenuates secretion through G(βγ) inhibition of Ca(2+) activity, while NPY activates a Ca(2+)-independent pathway mediated by G(α). GPCR ligands signal through multiple pathways to inhibit insulin secretion, and determining these mechanisms could lead to novel diabetic therapies.

Indexed as

AnimalsCalcium SignalingCells, CulturedDown-RegulationDrug Evaluation, PreclinicalGlucoseInsulinInsulin-Secreting CellsInsulin SecretionIslets of LangerhansMiceMice, Inbred C57BLNeuropeptide YSecretory PathwaySomatostatinTime FactorsGlucoseInsulinNeuropeptide YSomatostatin

Identifiers

PMID23211512
PMCPMC3543566
OpenAlexW2106467765

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.