Evidence map›Paper›PMID 38960128›Full record

ArticleMolecular metabolism2024

Deletion of miPEP in adipocytes protects against obesity and insulin resistance by boosting muscle metabolism.

Alexis Diaz-Vegas, Kristen C Cooke, Harry B Cutler, Belinda Yau, Stewart W C Masson, Dylan Harney, Oliver K Fuller, Meg Potter, Søren Madsen, Niamh R Craw and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular metabolism, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. The insulin signalling network.Nature metabolism · 2025
    Review
  2. Review
  3. 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

17 authors.

Alexis Diaz-VegasSchool of Life and Environmental Sciences, University of Sydney, Camperdown, New South Wales, Australia; Charles Perkins Centre, University of Sydney, Camperdown, New South Wales, Australia. Electronic address: alexis.diaz@sydney.edu.au.
Kristen C CookeSchool of Life and Environmental Sciences, University of Sydney, Camperdown, New South Wales, Australia; Charles Perkins Centre, University of Sydney, Camperdown, New South Wales, Australia.
Harry B CutlerSchool of Life and Environmental Sciences, University of Sydney, Camperdown, New South Wales, Australia; Charles Perkins Centre, University of Sydney, Camperdown, New South Wales, Australia.
Belinda YauSchool of Medical Sciences, University of Sydney, Camperdown, New South Wales, Australia.
Stewart W C MassonSchool of Life and Environmental Sciences, University of Sydney, Camperdown, New South Wales, Australia; Charles Perkins Centre, University of Sydney, Camperdown, New South Wales, Australia.
Dylan HarneySchool of Life and Environmental Sciences, University of Sydney, Camperdown, New South Wales, Australia; Charles Perkins Centre, University of Sydney, Camperdown, New South Wales, Australia.
Oliver K FullerSchool of Life and Environmental Sciences, University of Sydney, Camperdown, New South Wales, Australia; Charles Perkins Centre, University of Sydney, Camperdown, New South Wales, Australia.
Meg PotterSchool of Life and Environmental Sciences, University of Sydney, Camperdown, New South Wales, Australia; Charles Perkins Centre, University of Sydney, Camperdown, New South Wales, Australia.
Søren MadsenSchool of Life and Environmental Sciences, University of Sydney, Camperdown, New South Wales, Australia; Charles Perkins Centre, University of Sydney, Camperdown, New South Wales, Australia.
Niamh R CrawSchool of Life and Environmental Sciences, University of Sydney, Camperdown, New South Wales, Australia; Charles Perkins Centre, University of Sydney, Camperdown, New South Wales, Australia.
Yiju ZhangSchool of Life and Environmental Sciences, University of Sydney, Camperdown, New South Wales, Australia; Charles Perkins Centre, University of Sydney, Camperdown, New South Wales, Australia.
Cesar L MorenoSchool of Life and Environmental Sciences, University of Sydney, Camperdown, New South Wales, Australia; Charles Perkins Centre, University of Sydney, Camperdown, New South Wales, Australia.
Melkam A KebedeSchool of Medical Sciences, University of Sydney, Camperdown, New South Wales, Australia.
G Gregory NeelySchool of Life and Environmental Sciences, University of Sydney, Camperdown, New South Wales, Australia; Charles Perkins Centre, University of Sydney, Camperdown, New South Wales, Australia.
Jacqueline StöckliSchool of Life and Environmental Sciences, University of Sydney, Camperdown, New South Wales, Australia; Charles Perkins Centre, University of Sydney, Camperdown, New South Wales, Australia.
James G BurchfieldSchool of Life and Environmental Sciences, University of Sydney, Camperdown, New South Wales, Australia; Charles Perkins Centre, University of Sydney, Camperdown, New South Wales, Australia.
David E JamesSchool of Life and Environmental Sciences, University of Sydney, Camperdown, New South Wales, Australia; Charles Perkins Centre, University of Sydney, Camperdown, New South Wales, Australia; School of Medical Sciences, University of Sydney, Camperdown, New South Wales, Australia. Electronic address: david.james@sydney.edu.au.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria facilitate thousands of biochemical reactions, covering a broad spectrum of anabolic and catabolic processes. Here we demonstrate that the adipocyte mitochondrial proteome is markedly altered across multiple models of insulin resistance and reveal a consistent decrease in the level of the mitochondrial processing peptidase miPEP.

objectiveTo determine the role of miPEP in insulin resistance.

methodsTo experimentally test this observation, we generated adipocyte-specific miPEP knockout mice to interrogate its role in the aetiology of insulin resistance.

resultsWe observed a strong phenotype characterised by enhanced insulin sensitivity and reduced adiposity, despite normal food intake and physical activity. Strikingly, these phenotypes vanished when mice were housed at thermoneutrality, suggesting that metabolic protection conferred by miPEP deletion hinges upon a thermoregulatory process. Tissue specific analysis of miPEP deficient mice revealed an increment in muscle metabolism, and upregulation of the protein FBP2 that is involved in ATP hydrolysis in the gluconeogenic pathway.

conclusionThese findings suggest that miPEP deletion initiates a compensatory increase in skeletal muscle metabolism acting as a protective mechanism against diet-induced obesity and insulin resistance.

Indexed as

AdipocytesInsulin ResistanceMice, KnockoutMuscle, SkeletalObesityAnimalsMaleMiceMice, Inbred C57BLMitochondriaAdipose tissueInsulin resistanceMetabolismMitochondriaPeptidasesSkeletal muscle

Identifiers

PMID38960128
PMCPMC11292358

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.