Evidence map›Paper›PMID 37473754›Full record

ArticleCell metabolism2023

Liver mitochondrial cristae organizing protein MIC19 promotes energy expenditure and pedestrian locomotion by altering nucleotide metabolism.

Jee Hyung Sohn, Beste Mutlu, Pedro Latorre-Muro, Jiaxin Liang, Christopher F Bennett, Kfir Sharabi, Noa Kantorovich, Mark Jedrychowski, Steven P Gygi, Alexander S Banks and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Uridine.Trends in endocrinology and metabolism: TEM · 2026
    Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Molecular machineries shaping the mitochondrial inner membrane.Nature reviews. Molecular cell biology · 2025
    Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  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

11 authors at 3 institutions in 1 country.

Jee Hyung SohnDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA 02215, USA.
Beste MutluDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA 02215, USA.
Pedro Latorre-MuroDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA 02215, USA.
Jiaxin LiangDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA 02215, USA.
Christopher F BennettDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA 02215, USA.
Kfir SharabiDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA 02215, USA.
Noa KantorovichDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA 02215, USA.
Mark JedrychowskiDepartment of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA 02215, USA.
Steven P GygiDepartment of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA 02215, USA.
Alexander S BanksDivision of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.
Pere PuigserverDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA 02215, USA. Electronic address: pere_puigserver@dfci.harvard.edu.
Harvard University · USDana-Farber Cancer Institute · USBoston VA Research Institute · US

Funding

P&F programP30DK135043 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI Aaron S Leong · 2023 to 2026
$5.4M
Transcriptional Control of Mitochondrial Bioenergetic FunctionR01DK081418 · NIDDK · DANA-FARBER CANCER INST · PI PUIGSERVER, PERE · 2008 to 2021
$5.2M
Insulin Signaling and Metabolic Effects through CLK2 KinaseR01DK089883 · NIDDK · DANA-FARBER CANCER INST · PI PUIGSERVER, PERE · 2011 to 2020
$3.8M
Small molecules targeting hepatic glucose production and insulin resistanceR01DK117655 · NIDDK · DANA-FARBER CANCER INST · PI GRIFFIN, PATRICK ROBERT, PUIGSERVER, PERE · 2019 to 2023
$3.3M
Mechanisms of mitochondrial-ER communication during dietary and thermal induced stressK99DK133502 · NIDDK · DANA-FARBER CANCER INST · PI LATORRE MURO, PEDRO ANTONIO · 2023 to 2024
$180k
Remodeling mitochondrial cristae to rescue bioenergetic defects in mitochondrial diseaseF32GM136019 · NIGMS · DANA-FARBER CANCER INST · PI MUTLU, BESTE · 2020 to 2022
$154k
NIDDK NIH HHS K99 DK133502NIDDK NIH HHS P30 DK135043NIDDK NIH HHS R01 DK081418NIDDK NIH HHS R01 DK089883NIDDK NIH HHS R01 DK117655NIGMS NIH HHS F32 GM136019
6 · The paper itself

Abstract

Liver mitochondria undergo architectural remodeling that maintains energy homeostasis in response to feeding and fasting. However, the specific components and molecular mechanisms driving these changes and their impact on energy metabolism remain unclear. Through comparative mouse proteomics, we found that fasting induces strain-specific mitochondrial cristae formation in the liver by upregulating MIC19, a subunit of the MICOS complex. Enforced MIC19 expression in the liver promotes cristae formation, mitochondrial respiration, and fatty acid oxidation while suppressing gluconeogenesis. Mice overexpressing hepatic MIC19 show resistance to diet-induced obesity and improved glucose homeostasis. Interestingly, MIC19 overexpressing mice exhibit elevated energy expenditure and increased pedestrian locomotion. Metabolite profiling revealed that uracil accumulates in the livers of these mice due to increased uridine phosphorylase UPP2 activity. Furthermore, uracil-supplemented diet increases locomotion in wild-type mice. Thus, MIC19-induced mitochondrial cristae formation in the liver increases uracil as a signal to promote locomotion, with protective effects against diet-induced obesity.

Indexed as

Energy MetabolismLiverWalkingAnimalsDiet, High-FatMembrane ProteinsMiceMitochondria, LiverMitochondrial ProteinsProteomeUracilWeight GainChchd3 protein, mouseMembrane ProteinsMitochondrial ProteinsProteomeUracilbrisk walkingdiabetesfatty livermitochondrial cristaeobesityuracil

Identifiers

PMID37473754
PMCPMC10528355
OpenAlexW4384830561

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.