Evidence map›Paper›PMID 15175015›Full record

ArticleThe Biochemical journal2004

Kinetics and control of oxidative phosphorylation in rat liver mitochondria after dexamethasone treatment.

Damien Roussel, Jean-François Dumas, Gilles Simard, Yves Malthièry, Patrick Ritz

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 30% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. A meta-analysis of glucocorticoids as modulators of oxidative stress in vertebrates.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2011
    Pooled it
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  11. Lipid-induced thermogenesis is up-regulated by the first cold-water immersions in juvenile penguins.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2016
    Article
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  14. Article
  15. Insulin resistance is a cellular antioxidant defense mechanism.Proceedings of the National Academy of Sciences of the United States of America · 2009
    Article
  16. Effect of muramyl peptides on mitochondrial respiration.Clinical and experimental immunology · 2009
    Article
  17. Effects of corticosteroids on oxidative damage and circulating carotenoids in captive adult kestrels (Falco tinnunculus).Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2008
    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

5 authors at 1 institution in 1 country.

Damien RousselLaboratoire de Biochimie et Biologie Moléculaire, INSERM EMI-U 00.18, 4 rue Larrey, F-49033 Angers cedex, France.
Jean-François Dumas
Gilles Simard
Yves Malthièry
Patrick Ritz
Inserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present investigation was undertaken in order to evaluate the contributions of ATP synthesis and proton leak reactions to the rate of active respiration of liver mitochondria, which is altered following dexamethasone treatment (1.5 mg/kg per day for 5 days). We applied top-down metabolic control analysis and its extension, elasticity analysis, to gain insight into the mechanisms of glucocorticoid regulation of mitochondrial bioenergetics. Liver mitochondria were isolated from dexamethasone-treated, pair-fed and control rats when in a fed or overnight fasted state. Injection of dexamethasone for 5 days resulted in an increase in the fraction of the proton cycle of phosphorylating liver mitochondria, which was associated with a decrease in the efficiency of the mitochondrial oxidative phosphorylation process in liver. This increase in proton leak activity occurred with little change in the mitochondrial membrane potential, despite a significant decrease in the rate of oxidative phosphorylation. Regulation analysis indicates that mitochondrial membrane potential homoeostasis is achieved by equal inhibition of the mitochondrial substrate oxidation and phosphorylation reactions in rats given dexamethasone. Our results also suggest that active liver mitochondria from dexamethasone-treated rats are capable of maintaining phosphorylation flux for cellular purposes, despite an increase in the energetic cost of mitochondrial ATP production due to increased basal proton permeability of the inner membrane. They also provide a complete description of the effects of dexamethasone treatment on liver mitochondrial bioenergetics.

Indexed as

Adenosine TriphosphateAnimalsBody WeightDexamethasoneEatingEfficiencyFatty Acids, NonesterifiedKineticsLiverMaleMembrane PotentialsMitochondria, LiverOrgan SizeOxidation-ReductionOxidative PhosphorylationOxygen ConsumptionAdenosine TriphosphateDexamethasoneFatty Acids, NonesterifiedProton PumpsProtons

Identifiers

PMID15175015
PMCPMC1133805
OpenAlexW2071626849

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.