Evidence map›Paper›PMID 24911170›Full record

ArticlePloS one2014

Bistability in glycolysis pathway as a physiological switch in energy metabolism.

Bhanu Chandra Mulukutla, Andrew Yongky, Prodromos Daoutidis, Wei-Shou Hu

Abstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
–field-weighted citation impact
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

30 citing papers in PubMed.

  1. Article
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  10. Homeostasis in networks with multiple inputs.Journal of mathematical biology · 2024
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  12. Article
  13. Article
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  15. Article
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  17. Review
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  19. Stochastic Simulation of Cellular Metabolism.IEEE access : practical innovations, open solutions · 2020
    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.

Bhanu Chandra MulukutlaDepartment of Chemical Engineering and Materials Science, University of Minnesota, Minneapolis, Minnesota, United States of America.
Andrew YongkyDepartment of Chemical Engineering and Materials Science, University of Minnesota, Minneapolis, Minnesota, United States of America.
Prodromos DaoutidisDepartment of Chemical Engineering and Materials Science, University of Minnesota, Minneapolis, Minnesota, United States of America.
Wei-Shou HuDepartment of Chemical Engineering and Materials Science, University of Minnesota, Minneapolis, Minnesota, United States of America.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The flux of glycolysis is tightly controlled by feed-back and feed-forward allosteric regulations to maintain the body's glucose homeostasis and to respond to cell's growth and energetic needs. Using a mathematical model based on reported mechanisms for the allosteric regulations of the enzymes, we demonstrate that glycolysis exhibits multiple steady state behavior segregating glucose metabolism into high flux and low flux states. Two regulatory loops centering on phosphofructokinase and on pyruvate kinase each gives rise to the bistable behavior, and together impose more complex flux control. Steady state multiplicity endows glycolysis with a robust switch to transit between the two flux states. Under physiological glucose concentrations the glycolysis flux does not move between the states easily without an external stimulus such as hormonal, signaling or oncogenic cues. Distinct combination of isozymes in glycolysis gives different cell types the versatility in their response to different biosynthetic and energetic needs. Insights from the switch behavior of glycolysis may reveal new means of metabolic intervention in the treatment of cancer and other metabolic disorders through suppression of glycolysis.

Indexed as

Energy MetabolismGlycolysisModels, BiologicalFructosephosphatesHeLa CellsHumansIsoenzymesKineticsPhosphofructokinasesPyruvate Kinasefructose-6-phosphateFructosephosphatesIsoenzymesPhosphofructokinasesPyruvate Kinase

Identifiers

PMID24911170
PMCPMC4049617

What OpenQuestion holds

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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.