Evidence map›Paper›PMID 28452586›Full record

ReviewAdipocyte2017

Stress turns on the heat: Regulation of mitochondrial biogenesis and UCP1 by ROS in adipocytes.

Sara P Ortega, Edward T Chouchani, Sihem Boudina

Open access · goldAbstract readReview
In one paragraph

Review in Adipocyte, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

25 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Review
  3. Theranostics · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. The Role of microRNAs in Metabolic Syndrome-Related Oxidative Stress.International journal of molecular sciences · 2020
    Review
  16. Review
  17. Article
  18. Mitochondrial biogenesis: An update.Journal of cellular and molecular medicine · 2020
    Review
  19. Review
  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

3 authors at 2 institutions in 1 country.

Sara P Ortegaa Department of Nutrition and Integrative Physiology and Division of Endocrinology , Metabolism and Diabetes and Program in Molecular Medicine, University of Utah School of Medicine , Salt Lake City , Utah , USA.
Edward T Chouchanib Dana-Farber Cancer Institute & Department of Cell Biology, Harvard Medical School , Boston , Massachusetts , USA.
Sihem Boudinaa Department of Nutrition and Integrative Physiology and Division of Endocrinology , Metabolism and Diabetes and Program in Molecular Medicine, University of Utah School of Medicine , Salt Lake City , Utah , USA.
University of Utah · USHarvard University · US

Funding

Novel pathways for fat burning that protects from high fat diet-induced metabolicR01DK098646 · NIDDK · UNIVERSITY OF UTAH · PI BOUDINA, SIHEM · 2013 to 2017
$1.6M
Post-Developmental Adipocyte Autophagy in Control of Insulin-Glucose HomeostasisR01DK100826 · NIDDK · UNIVERSITY OF UTAH · PI BOUDINA, SIHEM · 2013 to 2017
$1.6M
NIDDK NIH HHS R01 DK098646NIDDK NIH HHS R01 DK100826
6 · The paper itself

Abstract

Reactive oxygen species (ROS) production and oxidative stress (OS) in adipose tissue are associated with obesity and insulin resistance (IR). The nature of this relationship i.e., cause and effect or consequence has not been clearly determined. We provide evidence that elevated mitochondrial ROS generated by adipocytes from mice with diet-induced obesity (DIO) represents an adaptive mechanism that precipitates fatty acid oxidation, mitochondrial biogenesis, and mitochondrial uncoupling in an effort to defend against weight gain. Consistent with that, mice with adipocyte-specific deletion of manganese superoxide dismutase (MnSOD) exhibit increased adipocyte superoxide generation and are protected from weight gain and insulin resistance which otherwise develops in wild-type (WT) mice that consume an obesogenic diet. The defense mechanism displayed by MnSOD-deficiency in fat cells appears to be mediated by a dual effect of ROS on inefficient substrate oxidation through uncoupling of oxidative phosphorylation and enhanced mitochondrial biogenesis. The aim of this commentary is to summarize and contextualize additional evidence supporting the importance of mitochondrial ROS in the regulation of mitochondrial biogenesis and the modulation of uncoupling protein 1 (UCP1) expression and activation in both white and brown adipocytes.

Indexed as

AdipocytesAnimalsEnergy MetabolismMiceMitochondriaMitochondrial ProteinsOrganelle BiogenesisOxidative StressReactive Oxygen SpeciesSuperoxide DismutaseUncoupling Protein 1Mitochondrial ProteinsReactive Oxygen SpeciesSuperoxide DismutaseUncoupling Protein 1brown adipose tissuemitochondriaMnSODoxidative modificationproton leakROSsuperoxideUncoupling protein 1 (UCP1)

Identifiers

PMID28452586
PMCPMC5358708
OpenAlexW2566068446

What OpenQuestion holds

Textmetadata
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.