Mitochondrial control of amino acid catabolism by a fasting-inducible mitochondrial carrier.

Satoshi Oikawa, Tadashi Yamamuro, Hiroshi Nishida, Daisuke Katoh, Dandan Wang, Masanori Fujimoto, Shingo Kajimura

Abstract read

In one paragraph

Article in Science advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it

0cells of the map it votes in

0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

7 authors.

Satoshi OikawaDivision of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Harvard Medical School, and Howard Hughes Medical Institute, Boston, MA, United States.ORCID 0000-0002-7696-8128

Tadashi YamamuroDivision of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Harvard Medical School, and Howard Hughes Medical Institute, Boston, MA, United States.ORCID 0000-0002-0610-5204

Hiroshi NishidaDivision of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Harvard Medical School, and Howard Hughes Medical Institute, Boston, MA, United States.ORCID 0000-0003-0284-5771

Daisuke KatohDivision of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Harvard Medical School, and Howard Hughes Medical Institute, Boston, MA, United States.ORCID 0000-0001-6576-0463

Dandan WangDivision of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Harvard Medical School, and Howard Hughes Medical Institute, Boston, MA, United States.ORCID 0009-0006-2788-7475

Masanori FujimotoDivision of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Harvard Medical School, and Howard Hughes Medical Institute, Boston, MA, United States.ORCID 0000-0003-1458-8207

Shingo KajimuraDivision of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Harvard Medical School, and Howard Hughes Medical Institute, Boston, MA, United States.ORCID 0000-0003-0672-5910

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic adaptation to nutrient deprivation requires coordinated control of mitochondrial anaplerosis and cataplerosis; however, how metabolite flux across the mitochondrial membrane is regulated during fasting remains less defined. Here, we report SLC25A34 as a fasting-inducible mitochondrial carrier that is highly expressed in oxidative skeletal muscle. Using bacterial reconstitution, proteo-liposomes, and tracer studies, we showed that SLC25A34 mediates the import of phosphoenolpyruvate (PEP) into the mitochondrial matrix. Loss of SLC25A34 impaired glutamine-supported anaplerosis under nutrient-deprived conditions, while glucose and pyruvate utilization remained largely intact. Muscle-specific deletion of

Indexed as

Amino AcidsFastingMitochondriaAnimalsMechanistic Target of Rapamycin Complex 1MiceMuscle, SkeletalSignal TransductionAmino AcidsMechanistic Target of Rapamycin Complex 1

Identifiers

PMID42536745

DOI10.1126/sciadv.aef0140

PMCPMC13426421

What Socratic holds

Textmetadata

LicenceCC BY

Read underepoch 390

Registered trials

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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 Socratic graph.