Evidence map›Paper›PMID 40968275›Full record

ArticleNature metabolism2025

Redox-dependent liver gluconeogenesis impacts different intensity exercise in mice.

Takahiro Horiuchi, Keizo Kaneko, Shinichiro Hosaka, Kenji Uno, Seitaro Tomiyama, Kei Takahashi, Maya Yamato, Akira Endo, Hiroto Sugawara, Yohei Kawana and 11 more

Abstract read
In one paragraph

Article in Nature metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Review
  3. Temporal Metabolomics Profiling Reveals Liver Metabolic Control in Single and Repeated Exhaustive Exercise in Murine Models.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  4. Review
  5. 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

21 authors.

Takahiro HoriuchiDepartment of Diabetes, Metabolism and Endocrinology, Tohoku University Graduate School of Medicine, Sendai, Japan.ORCID http://orcid.org/0000-0002-1907-2042
Keizo KanekoDepartment of Diabetes, Metabolism and Endocrinology, Tohoku University Graduate School of Medicine, Sendai, Japan. kayzo@oak.dti.ne.jp.ORCID http://orcid.org/0000-0003-1612-7957
Shinichiro HosakaDepartment of Diabetes, Metabolism and Endocrinology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Kenji UnoDivision of Endocrinology and Metabolism, Department of Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan.
Seitaro TomiyamaDepartment of Diabetes, Metabolism and Endocrinology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Kei TakahashiDepartment of Diabetes, Metabolism and Endocrinology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Maya YamatoDepartment of Diabetes, Metabolism and Endocrinology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Akira EndoDepartment of Diabetes, Metabolism and Endocrinology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Hiroto SugawaraDepartment of Diabetes, Metabolism and Endocrinology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Yohei KawanaDepartment of Diabetes, Metabolism and Endocrinology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Yoichiro AsaiDepartment of Diabetes, Metabolism and Endocrinology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Shinjiro KodamaDepartment of Diabetes, Metabolism and Endocrinology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Junta ImaiDepartment of Diabetes, Metabolism and Endocrinology, Tohoku University Graduate School of Medicine, Sendai, Japan.ORCID http://orcid.org/0000-0003-4636-5905
Seiya MizunoLaboratory Animal Resource Center and Transborder Medical Research Center, Institute of Medicine, University of Tsukuba, Tsukuba, Japan.ORCID http://orcid.org/0000-0002-6740-5817
Satoru TakahashiLaboratory Animal Resource Center and Transborder Medical Research Center, Institute of Medicine, University of Tsukuba, Tsukuba, Japan.ORCID http://orcid.org/0000-0002-8540-7760
Atsushi TakasakiDepartment of Endocrinology, Hematology and Gerontology, Chiba University Graduate School of Medicine, Chiba, Japan.
Hiraku OnoDepartment of Endocrinology, Hematology and Gerontology, Chiba University Graduate School of Medicine, Chiba, Japan.
Koutaro YokoteChiba University, Chiba, Japan.
Rae MaedaMultiomics Platform, Center for Cancer Immunotherapy and Immunobiology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Yuki SugiuraMultiomics Platform, Center for Cancer Immunotherapy and Immunobiology, Kyoto University Graduate School of Medicine, Kyoto, Japan.ORCID http://orcid.org/0000-0002-6983-8958
Hideki KatagiriDepartment of Diabetes, Metabolism and Endocrinology, Tohoku University Graduate School of Medicine, Sendai, Japan. hideki.katagiri.e1@tohoku.ac.jp.ORCID http://orcid.org/0000-0003-1093-3704

Funding

MEXT | Japan Science and Technology Agency (JST) JPMJMS2023MEXT | Japan Society for the Promotion of Science (JSPS) 20H05694MEXT | Japan Society for the Promotion of Science (JSPS) 22K08642
6 · The paper itself

Abstract

Hepatic gluconeogenesis produces glucose from various substrates to meet energy demands. However, how these substrates are preferentially used under different conditions remains unclear. Here, we show that preferential supplies of lactate and glycerol modulate hepatic gluconeogenesis, thereby impacting high-intensity and low-intensity exercise capacities, respectively. We find that liver-specific knockout of phosphoenolpyruvate carboxykinase 1 (L-Pck1KO), which blocks gluconeogenesis from lactate, decreases high-intensity exercise capacity but increases low-intensity exercise capacity by enhancing gluconeogenesis from glycerol. Conversely, liver-specific knockout of glycerol kinase (L-GykKO), which inhibits glycerol-derived gluconeogenesis, induces the opposite effects by enhancing gluconeogenesis from lactate. Given that these compensatory steps depend on NAD

Indexed as

GluconeogenesisLiverPhysical Conditioning, AnimalAnimalsGlucoseGlycerolLactic AcidMaleMiceMice, Inbred C57BLMice, KnockoutOxidation-ReductionGlucoseGlycerolLactic Acid

Identifiers

PMID40968275
PMCPMC12552127

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.