Evidence map›Paper›PMID 35687590›Full record

ArticlePLoS biology2022

The polyol pathway is an evolutionarily conserved system for sensing glucose uptake.

Hiroko Sano, Akira Nakamura, Mariko Yamane, Hitoshi Niwa, Takashi Nishimura, Kimi Araki, Kazumasa Takemoto, Kei-Ichiro Ishiguro, Hiroki Aoki, Yuzuru Kato and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PLoS biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Cytoplasmic fluidity couples nutrient availability and enterocyte fate in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
  4. Review
  5. Lipid Metabolism in Relation to Carbohydrate Metabolism.Advances in experimental medicine and biology · 2026
    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

11 authors at 4 institutions in 1 country.

Hiroko SanoDepartment of Molecular Genetics, Institute of Life Science, Kurume University, Kurume, Fukuoka, Japan.ORCID 0000-0001-9834-647X
Akira NakamuraDepartment of Germline Development, Institute of Molecular Embryology and Genetics, and Graduate School of Pharmaceutical Sciences, Kumamoto University, Kumamoto, Kumamoto, Japan.
Mariko YamaneDepartment of Pluripotent Stem Cell Biology, Institute of Molecular Embryology and Genetics, and Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Kumamoto, Japan.
Hitoshi NiwaDepartment of Pluripotent Stem Cell Biology, Institute of Molecular Embryology and Genetics, and Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Kumamoto, Japan.
Takashi NishimuraLaboratory of Metabolic Regulation and Genetics, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma, Japan.
Kimi ArakiInstitute of Resource Development and Analysis, Kumamoto University, Kumamoto, Kumamoto, Japan.
Kazumasa TakemotoInstitute of Resource Development and Analysis, Kumamoto University, Kumamoto, Kumamoto, Japan.
Kei-Ichiro IshiguroDepartment of Chromosome Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Kumamoto, Japan.
Hiroki AokiCardiovascular Research Institute, Kurume University, Kurume, Fukuoka, Japan.
Yuzuru KatoMammalian Development Laboratory, Department of Gene Function and Phenomics, National Institute of Genetics, Mishima, Shizuoka, Japan.
Masayasu KojimaDepartment of Molecular Genetics, Institute of Life Science, Kurume University, Kurume, Fukuoka, Japan.
Kumamoto University · JPKurume University · JPGunma University · JPNational Institute of Genetics · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cells must adjust the expression levels of metabolic enzymes in response to fluctuating nutrient supply. For glucose, such metabolic remodeling is highly dependent on a master transcription factor ChREBP/MondoA. However, it remains elusive how glucose fluctuations are sensed by ChREBP/MondoA despite the stability of major glycolytic pathways. Here, we show that in both flies and mice, ChREBP/MondoA activation in response to glucose ingestion involves an evolutionarily conserved glucose-metabolizing pathway: the polyol pathway. The polyol pathway converts glucose to fructose via sorbitol. It has been believed that this pathway is almost silent, and its activation in hyperglycemic conditions has deleterious effects on human health. We show that the polyol pathway regulates the glucose-responsive nuclear translocation of Mondo, a Drosophila homologue of ChREBP/MondoA, which directs gene expression for organismal growth and metabolism. Likewise, inhibition of the polyol pathway in mice impairs ChREBP's nuclear localization and reduces glucose tolerance. We propose that the polyol pathway is an evolutionarily conserved sensing system for glucose uptake that allows metabolic remodeling.

Indexed as

Basic Helix-Loop-Helix Leucine Zipper Transcription FactorsGlucoseAnimalsCarbohydrate MetabolismDrosophilaMicePolymersTranscription FactorsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsGlucoseMondoA protein, mousePolymerspolyolTranscription Factors

Identifiers

PMID35687590
PMCPMC9223304
OpenAlexW4281816910

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.