Evidence map›Paper›PMID 29773871›Full record

ReviewNature reviews. Endocrinology2018

The somatostatin-secreting pancreatic δ-cell in health and disease.

Patrik Rorsman, Mark O Huising

Open access · greenAbstract readComparative StudyReview
In one paragraph

Review in Nature reviews. Endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 158 papers.

0numbers the graph read from it
0cells of the map it votes in
158citing papers in PubMed
21.8field-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

158 citing papers in PubMed, 243 citations in OpenAlex.

  1. Trial
  2. Postnatal refinement of CaChannels (Austin, Tex.) · 2026
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  14. Conserved Molecular Responses to Arsenite Exposure inbioRxiv : the preprint server for biology · 2026
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98 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 2 countries.

Patrik RorsmanOxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine, Churchill Hospital, University of Oxford, Oxford, UK. Patrik.rorsman@drl.ox.ac.uk.
Mark O HuisingDepartment of Neurobiology, Physiology and Behavior, College of Biological Sciences, University of California, Davis, Davis, CA, USA.
Oxford Centre for Diabetes, Endocrinology and Metabolism · GBUniversity of California, Davis · US

Funding

PARACRINE FEEDBACK BY PANCREATIC DELTA CELLS TO CONTROL GLUCAGON AND INSULIN RELEASE AND MANAGE DIABETESR01DK110276 · NIDDK · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Mark O. Huising · 2017 to 2026
$3.9M
NIDDK NIH HHS R01 DK110276Wellcome Trust 095531/Z/11/Z
6 · The paper itself

Abstract

The somatostatin-secreting δ-cells comprise ~5% of the cells of the pancreatic islets. The δ-cells have complex morphology and might interact with many more islet cells than suggested by their low numbers. δ-Cells contain ATP-sensitive potassium channels, which open at low levels of glucose but close when glucose is elevated. This closure initiates membrane depolarization and electrical activity and increased somatostatin secretion. Factors released by neighbouring α-cells or β-cells amplify the glucose-induced effects on somatostatin secretion from δ-cells, which act locally within the islets as paracrine or autocrine inhibitors of insulin, glucagon and somatostatin secretion. The effects of somatostatin are mediated by activation of somatostatin receptors coupled to the inhibitory G protein, which culminates in suppression of the electrical activity and exocytosis in α-cells and β-cells. Somatostatin secretion is perturbed in animal models of diabetes mellitus, which might explain the loss of appropriate hypoglycaemia-induced glucagon secretion, a defect that could be mitigated by somatostatin receptor 2 antagonists. Somatostatin antagonists or agents that suppress somatostatin secretion have been proposed as an adjunct to insulin therapy. In this Review, we summarize the cell physiology of somatostatin secretion, what might go wrong in diabetes mellitus and the therapeutic potential of agents targeting somatostatin secretion or action.

Indexed as

AnimalsBiomarkersCase-Control StudiesDiabetes MellitusFemaleGlucagonHumansHypoglycemiaMalePrognosisReceptors, SomatostatinReference ValuesSomatostatinSomatostatin-Secreting CellsTreatment OutcomeBiomarkersGlucagonReceptors, SomatostatinSomatostatinSSTR2 protein, human

Identifiers

PMID29773871
PMCPMC5997567
OpenAlexW2803302591

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.