Evidence map›Paper›PMID 23426361›Full record

ArticleThe Journal of biological chemistry2013

Metabolome response to glucose in the β-cell line INS-1 832/13.

Matthew A Lorenz, Mahmoud A El Azzouny, Robert T Kennedy, Charles F Burant

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
9.0field-weighted citation impact, top 2% 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

60 citing papers in PubMed, 134 citations in OpenAlex.

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  13. Monitoring glycolytic dynamics in single cells using a fluorescent biosensor for fructose 1,6-bisphosphate.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  14. Review
  15. Review
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  18. The Pancreatic β-Cell: The Perfect Redox System.Antioxidants (Basel, Switzerland) · 2021
    Review
  19. Article
  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

4 authors at 1 institution in 1 country.

Matthew A LorenzDepartment of Chemistry, University of Michigan, Ann Arbor, Michigan 48105, USA.
Mahmoud A El Azzouny
Robert T Kennedy
Charles F Burant
University of Michigan–Ann Arbor · US

Funding

PUBLIC HEALTH DEMONSTRATIONP60DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MYERS, MARTIN G · 1985 to 2012
$26.5M
Pilot and Feasibility (P and F) ProgramP30DK089503 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Kanakadurga Singer · 2010 to 2026
$20.3M
Statistics and Bioinformatics Core - WangU24DK097153 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BURANT, CHARLES F · 2012 to 2017
$10.1M
MICROELECTRODE AND MICRODIALYSIS-BASED INSULIN SENSORSR01DK046960 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KENNEDY, ROBERT T · 1993 to 2020
$3.3M
Design and Use of Methods for Peptide Secretion Studies - Diversity SupplementR37DK046960 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KENNEDY, ROBERT T · 2006 to 2015
$3.0M
Using Systems Biology to Understand Islet Adaptation and Failure DiabetesR01DK079084 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BURANT, CHARLES F · 2007 to 2010
$2.1M
NIDDK NIH HHS DK046960NIDDK NIH HHS DK079084NIDDK NIH HHS P30 DK089503NIDDK NIH HHS P60 DK020572NIDDK NIH HHS P60 DK20572NIDDK NIH HHS R01 DK046960NIDDK NIH HHS R01 DK079084NIDDK NIH HHS R37 DK046960NIDDK NIH HHS U24 DK097153
6 · The paper itself

Abstract

Glucose-stimulated insulin secretion (GSIS) from pancreatic β-cells is triggered by metabolism of the sugar to increase ATP/ADP ratio that blocks the KATP channel leading to membrane depolarization and insulin exocytosis. Other metabolic pathways believed to augment insulin secretion have yet to be fully elucidated. To study metabolic changes during GSIS, liquid chromatography with mass spectrometry was used to determine levels of 87 metabolites temporally following a change in glucose from 3 to 10 mM glucose and in response to increasing concentrations of glucose in the INS-1 832/13 β-cell line. U-[(13)C]Glucose was used to probe flux in specific metabolic pathways. Results include a rapid increase in ATP/ADP, anaplerotic tricarboxylic acid cycle flux, and increases in the malonyl CoA pathway, support prevailing theories of GSIS. Novel findings include that aspartate used for anaplerosis does not derive from the glucose fuel added to stimulate insulin secretion, glucose flux into glycerol-3-phosphate, and esterification of long chain CoAs resulting in rapid consumption of long chain CoAs and de novo generation of phosphatidic acid and diacylglycerol. Further, novel metabolites with potential roles in GSIS such as 5-aminoimidazole-4-carboxamide ribotide (ZMP), GDP-mannose, and farnesyl pyrophosphate were found to be rapidly altered following glucose exposure.

Indexed as

Acyl Coenzyme AAnimalsCell LineEnergy MetabolismGlucoseInsulinInsulin-Secreting CellsInsulin SecretionLipid MetabolismMetabolomeMiceSweetening AgentsAcyl Coenzyme AGlucoseInsulinSweetening Agents

Identifiers

PMID23426361
PMCPMC3624472
OpenAlexW2080863876

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.