Evidence map›Paper›PMID 22389505›Full record

ArticleThe Journal of biological chemistry2012

Sphingosine 1-phosphate (S1P) regulates glucose-stimulated insulin secretion in pancreatic beta cells.

Jamie Cantrell Stanford, Andrew J Morris, Manjula Sunkara, Gabriel J Popa, Kara L Larson, Sabire Özcan

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.

  1. Pooled it
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  8. Sphingosine 1-Phosphate Regulates Obesity and Glucose Homeostasis.International journal of molecular sciences · 2024
    Review
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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

6 authors at 1 institution in 1 country.

Jamie Cantrell StanfordDepartment of Molecular and Cellular Biochemistry, University of Kentucky, Lexington, Kentucky 40536, USA.
Andrew J Morris
Manjula Sunkara
Gabriel J Popa
Kara L Larson
Sabire Özcan
University of Kentucky · US

Funding

UNDERSTANDING THE MOLECULAR BASIS OF EPIGENETIC TRANSCRIPTIONAL SILENCINGP20RR020171 · NCRR · UNIVERSITY OF KENTUCKY · PI PAUMI, CHRISTIAN M · 2004 to 2011
$16.5M
Histone Acetylation and Insulin Gene ExpressionR01DK067581 · NIDDK · UNIVERSITY OF KENTUCKY · PI OZCAN, SABIRE · 2005 to 2010
$1.5M
Thermo/Finnigan TSQ AM Triple Stage Quadrupole Mass SpectrometerS10RR024598 · NCRR · UNIVERSITY OF KENTUCKY · PI MORRIS, ANDREW J · 2008 to 2008
$493k
Beta-Cell Transcription Factors and Insulin Gene ExpressionR56DK067581 · NIDDK · UNIVERSITY OF KENTUCKY · PI OZCAN, SABIRE · 2010 to 2010
$223k
NCRR NIH HHS P20 RR020171NCRR NIH HHS P20RR020171NCRR NIH HHS S10 RR024598NIDDK NIH HHS DK067581NIDDK NIH HHS R01 DK067581NIDDK NIH HHS R56 DK067581
6 · The paper itself

Abstract

Recent studies suggest that sphingolipid metabolism is altered during type 2 diabetes. Increased levels of the sphingolipid ceramide are associated with insulin resistance. However, a role for sphingolipids in pancreatic beta cell function, or insulin production, and release remains to be established. Our studies in MIN6 cells and mouse pancreatic islets demonstrate that glucose stimulates an intracellular rise in the sphingolipid, sphingosine 1-phosphate (S1P), whereas the levels of ceramide and sphingomyelin remain unchanged. The increase in S1P levels by glucose is due to activation of sphingosine kinase 2 (SphK2). Interestingly, rises in S1P correlate with increased glucose-stimulated insulin secretion (GSIS). Decreasing S1P levels by treatment of MIN6 cells or primary islets with the sphingosine kinase inhibitor reduces GSIS. Moreover, knockdown of SphK2 alone results in decreased GSIS, whereas knockdown of the S1P phosphatase, Sgpp1, leads to a rise in GSIS. Treatment of mice with the sphingosine kinase inhibitor impairs glucose disposal due to decreased plasma insulin levels. Altogether, our data suggest that glucose activates SphK2 in pancreatic beta cells leading to a rise in S1P levels, which is important for GSIS.

Indexed as

AnimalsCell Line, TumorGlucoseGlucose IntoleranceGlucose Tolerance TestInjections, IntraperitonealInsulinInsulinomaInsulin-Secreting CellsInsulin SecretionLysophospholipidsMiceMice, Inbred C57BLPancreatic NeoplasmsPhosphoric Monoester HydrolasesPhosphotransferases (Alcohol Group Acceptor)GlucoseInsulinLysophospholipidsPhosphoric Monoester HydrolasesPhosphotransferases (Alcohol Group Acceptor)RNA, Small InterferingSphingosinesphingosine 1-phosphateSphingosine Kinase

Identifiers

PMID22389505
PMCPMC3339968
OpenAlexW2131629629

What OpenQuestion 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 OpenQuestion graph.