Evidence map›Paper›PMID 1674863›Full record

ArticleThe Biochemical journal1991

Mechanisms of the stimulation of insulin release by oxytocin in normal mouse islets.

Z Y Gao, G Drews, J C Henquin

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Oxytocin: A Potential Therapeutic for Obesity.Journal of obesity & metabolic syndrome · 2021
    Review
  6. Article
  7. Review
  8. TheDiabetes, metabolic syndrome and obesity : targets and therapy · 2019
    Article
  9. Oxytocin in metabolic homeostasis: implications for obesity and diabetes management.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2019
    Review
  10. Review
  11. Review
  12. Article
  13. Opposing crosstalk between leptin and glucocorticoids rapidly modulates synaptic excitation via endocannabinoid release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006
    Article
  14. Article
  15. 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.

Z Y GaoUnité de Diabétologie et Nutrition, University of Louvain Faculty of Medicine, Brussels, Belgium.
G Drews
J C Henquin

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxytocin (OT) produced a dose-dependent increase in somatostatin, glucagon and insulin release by isolated mouse islets. A small effect on somatostatin release was observed with 0.1 nM-OT, but 1-10 nM-OT was required to affect A- and B- cells significantly. The effects of OT on somatostatin and glucagon release were similar in the presence of 3 mM- and 10 mM-glucose. No change in insulin release was produced by OT in 3 mM-glucose, but a stimulation was still observed in the presence of a maximally effective concentration of glucose (30 mM). The increase in insulin release produced by OT (in 15 mM-glucose) was accompanied by small accelerations of 86Rb and 45Ca efflux from islet cells. Omission of extracellular Ca2+ accentuated the effect of OT on 86Rb efflux, attenuated that on 45Ca efflux, and abolished that on release. OT never inhibited 86Rb efflux. It did not affect the resting potential of B-cells, but slightly increased the Ca2(+)-dependent electrical activity induced by 15 mM-glucose. OT did not affect cyclic AMP levels, but increased inositol phosphate levels in islet cells. It is suggested that the amplification of glucose-induced insulin release that OT produces is due to a stimulation of phosphoinositide metabolism, and presumably an activation of protein kinase C, rather than to a change in cyclic AMP levels or a direct action on the membrane potential. Since OT is present in the pancreas, it is possible that it exerts a neuropeptidergic control of the islet function.

Indexed as

AnimalsCalciumCyclic AMPDose-Response Relationship, DrugFemaleGlucagonGlucoseInositolInositol PhosphatesInsulinInsulin SecretionIn Vitro TechniquesIslets of LangerhansKineticsMembrane PotentialsMiceCalciumCyclic AMPGlucagonGlucoseInositolInositol PhosphatesInsulinOxytocinRubidiumSomatostatin

Identifiers

PMID1674863
PMCPMC1151160
OpenAlexW1709065996

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.