Evidence map›Paper›PMID 19961265›Full record

ReviewUpsala journal of medical sciences2009

Pulsatility of insulin release--a clinically important phenomenon.

Bo Hellman

Open access · diamondAbstract readReview
In one paragraph

Review in Upsala journal of medical sciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 2 pooled it
3.5field-weighted citation impact, top 8% 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

31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 77 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
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  8. Review
  9. Article
  10. Dynamic changes in β-cell [CaMolecular metabolism · 2022
    Article
  11. Article
  12. Article
  13. Article
  14. Role of Phosphodiesterase in the Biology and Pathology of Diabetes.International journal of molecular sciences · 2020
    Review
  15. Article
  16. Mathematical Modelling of Endocrine Systems.Trends in endocrinology and metabolism: TEM · 2019
    Review
  17. Article
  18. Article
  19. Review
  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

1 author at 1 institution in 1 country.

Bo HellmanDepartment of Medical Cell Biology, Uppsala University, Uppsala, Sweden. Bo.Hellman@mcb.uu.se
Uppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mechanisms and clinical importance of pulsatile insulin release are presented against the background of more than half a century of companionship with the islets of Langerhans. The insulin-secreting beta-cells are oscillators with intrinsic variations of cytoplasmic ATP and Ca(2+). Within the islets the beta-cells are mutually entrained into a common rhythm by gap junctions and diffusible factors (ATP). Synchronization of the different islets in the pancreas is supposed to be due to adjustment of the oscillations to the same phase by neural output of acetylcholine and ATP. Studies of hormone secretion from the perfused pancreas of rats and mice revealed that glucose induces pulses of glucagon anti-synchronous with pulses of insulin and somatostatin. The anti-synchrony may result from a paracrine action of somatostatin on the glucagon-producing alpha-cells. Purinoceptors have a key function for pulsatile release of islet hormones. It was possible to remove the glucagon and somatostatin pulses with maintenance of those of insulin with an inhibitor of the P2Y(1) receptors. Knock-out of the adenosine A(1) receptor prolonged the pulses of glucagon and somatostatin without affecting the duration of the insulin pulses. Studies of isolated human islets indicate similar relations between pulses of insulin, glucagon, and somatostatin as found during perfusion of the rodent pancreas. The observation of reversed cycles of insulin and glucagon adds to the understanding how the islets regulate hepatic glucose production. Current protocols for pulsatile intravenous infusion therapy (PIVIT) should be modified to mimic the anti-synchrony between insulin and glucagon normally seen in the portal blood.

Indexed as

Adenosine TriphosphateAnimalsBiological ClocksCalcium SignalingCell CommunicationGlucagonGlucoseHumansInsulinInsulin-Secreting CellsInsulin SecretionIn Vitro TechniquesMiceModels, BiologicalRatsSomatostatinAdenosine TriphosphateGlucagonGlucoseInsulinSomatostatin

Identifiers

PMID19961265
PMCPMC2852781
OpenAlexW1978045340

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.