Evidence map›Paper›PMID 21505151›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2011

Plasma membrane electron transport in pancreatic β-cells is mediated in part by NQO1.

Joshua P Gray, Timothy Eisen, Gary W Cline, Peter J S Smith, Emma Heart

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Mechanisms of Doxorubicin Toxicity in Pancreatic β-Cells.Toxicological sciences : an official journal of the Society of Toxicology · 2016
    Article
  10. Calorie restriction as an intervention in ageing.The Journal of physiology · 2016
    Review
  11. Article
  12. Sirtuin activation: a role for plasma membrane in the cell growth puzzle.The journals of gerontology. Series A, Biological sciences and medical sciences · 2013
    Article
  13. NAD kinase regulates the size of the NADPH pool and insulin secretion in pancreatic β-cells.American journal of physiology. Endocrinology and metabolism · 2012
    Article
  14. 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

5 authors at 4 institutions in 2 countries.

Joshua P GrayUnited States Coast Guard Academy, New London, Connecticut, USA.
Timothy Eisen
Gary W Cline
Peter J S Smith
Emma Heart
Brown University · USUnited States Coast Guard Academy · USUniversity of Southampton · GBYale University · US

Funding

VOLTAMMETRIC DETECTION OF METAL IONSP41RR001395 · NCRR · MARINE BIOLOGICAL LABORATORY · PI SMITH, PETER JS · 1985 to 2010
$12.7M
Metabolic and Mitochondrial Defects of Islet beta-cells of MODY-3R01DK071071 · NIDDK · YALE UNIVERSITY · PI CLINE, GARY W · 2005 to 2009
$1.0M
Role of islet structure and functionR21DK063984 · NIDDK · MARINE BIOLOGICAL LABORATORY · PI SMITH, PETER JS · 2003 to 2004
$310k
PLASMA MEMBRANE ELECTRON TRANSPORT AS A CONNECTOR OF THE BETA CELL METABOLIC CIRCR56DK088093 · NIDDK · MARINE BIOLOGICAL LABORATORY · PI HEART, EMMA · 2010 to 2010
$233k
NCRR NIH HHS P41-RR-001395NIDDK NIH HHS DK-063984NIDDK NIH HHS DK-071071NIDDK NIH HHS R56DK-088093
6 · The paper itself

Abstract

Plasma membrane electron transport (PMET), a cytosolic/plasma membrane analog of mitochondrial electron transport, is a ubiquitous system of cytosolic and plasma membrane oxidoreductases that oxidizes cytosolic NADH and NADPH and passes electrons to extracellular targets. While PMET has been shown to play an important role in a variety of cell types, no studies exist to evaluate its function in insulin-secreting cells. Here we demonstrate the presence of robust PMET activity in primary islets and clonal β-cells, as assessed by the reduction of the plasma membrane-impermeable dyes WST-1 and ferricyanide. Because the degree of metabolic function of β-cells (reflected by the level of insulin output) increases in a glucose-dependent manner between 4 and 10 mM glucose, PMET was evaluated under these conditions. PMET activity was present at 4 mM glucose and was further stimulated at 10 mM glucose. PMET activity at 10 mM glucose was inhibited by the application of the flavoprotein inhibitor diphenylene iodonium and various antioxidants. Overexpression of cytosolic NAD(P)H-quinone oxidoreductase (NQO1) increased PMET activity in the presence of 10 mM glucose while inhibition of NQO1 by its inhibitor dicoumarol abolished this activity. Mitochondrial inhibitors rotenone, antimycin A, and potassium cyanide elevated PMET activity. Regardless of glucose levels, PMET activity was greatly enhanced by the application of aminooxyacetate, an inhibitor of the malate-aspartate shuttle. We propose a model for the role of PMET as a regulator of glycolytic flux and an important component of the metabolic machinery in β-cells.

Indexed as

Adenosine TriphosphateAnimalsAntioxidantsCell MembraneCells, CulturedDose-Response Relationship, DrugElectron TransportEnzyme InhibitorsGlucoseInsulinInsulin-Secreting CellsInsulin SecretionMaleMiceMitochondriaModels, BiologicalAdenosine TriphosphateAntioxidantsEnzyme InhibitorsGlucoseInsulinNADNAD(P)H Dehydrogenase (Quinone)Nqo1 protein, mouse

Identifiers

PMID21505151
PMCPMC3129843
OpenAlexW2000571734

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.