Evidence map›Paper›PMID 27814396›Full record

ArticlePloS one2016

Chronic Activation of Hepatic Nrf2 Has No Major Effect on Fatty Acid and Glucose Metabolism in Adult Mice.

Sebastian Brachs, Angelika F Winkel, James Polack, Hui Tang, Maria Brachs, Daniel Margerie, Bodo Brunner, Kerstin Jahn-Hofmann, Hartmut Ruetten, Joachim Spranger and 1 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-weighted citation impact, top 25% 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

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Sebastian BrachsDepartment of Endocrinology, Diabetes and Nutrition, Center for Cardiovascular Research, Charité -University School of Medicine, Berlin, Germany.ORCID http://orcid.org/0000-0002-6336-3939
Angelika F WinkelSanofi-Aventis Deutschland GmbH, Industriepark Hoechst, Frankfurt am Main, Germany.
James PolackDepartment of Endocrinology, Diabetes and Nutrition, Center for Cardiovascular Research, Charité -University School of Medicine, Berlin, Germany.
Hui TangDepartment of Endocrinology, Diabetes and Nutrition, Center for Cardiovascular Research, Charité -University School of Medicine, Berlin, Germany.
Maria BrachsDepartment of Endocrinology, Diabetes and Nutrition, Center for Cardiovascular Research, Charité -University School of Medicine, Berlin, Germany.
Daniel MargerieSanofi-Aventis Deutschland GmbH, Industriepark Hoechst, Frankfurt am Main, Germany.
Bodo BrunnerSanofi-Aventis Deutschland GmbH, Industriepark Hoechst, Frankfurt am Main, Germany.
Kerstin Jahn-HofmannSanofi-Aventis Deutschland GmbH, Industriepark Hoechst, Frankfurt am Main, Germany.
Hartmut RuettenSanofi-Aventis Deutschland GmbH, Industriepark Hoechst, Frankfurt am Main, Germany.
Joachim SprangerDepartment of Endocrinology, Diabetes and Nutrition, Center for Cardiovascular Research, Charité -University School of Medicine, Berlin, Germany.
Dieter SchmollSanofi-Aventis Deutschland GmbH, Industriepark Hoechst, Frankfurt am Main, Germany.
Sanofi (Germany) · DEGerman Centre for Cardiovascular Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription factor NF-E2-related factor 2 (Nrf2) induces cytoprotective genes, but has also been linked to the regulation of hepatic energy metabolism. In order to assess the pharmacological potential of hepatic Nrf2 activation in metabolic disease, Nrf2 was activated over 7 weeks in mice on Western diet using two different siRNAs against kelch-like ECH-associated protein 1 (Keap1), the inhibitory protein of Nrf2. Whole genome expression analysis followed by pathway analysis demonstrated successful knock-down of Keap1 expression and induction of Nrf2-dependent genes involved in anti-oxidative stress defense and biotransformation, proving the activation of Nrf2 by the siRNAs against Keap1. Neither the expression of fatty acid- nor carbohydrate-handling proteins was regulated by Keap1 knock-down. Metabolic profiling of the animals did also not show effects on plasma and hepatic lipids, energy expenditure or glucose tolerance. The data indicate that hepatic Keap1/Nrf2 is not a major regulator of glucose or lipid metabolism in mice.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCarbohydrate MetabolismCytoskeletal ProteinsFatty AcidsGlucoseIntracellular Signaling Peptides and ProteinsKelch-Like ECH-Associated Protein 1Lipid MetabolismMaleMiceMice, Inbred C57BLNF-E2-Related Factor 2Oxidative StressSignal TransductionAdaptor Proteins, Signal TransducingCytoskeletal ProteinsFatty AcidsGlucoseIntracellular Signaling Peptides and ProteinsKelch-Like ECH-Associated Protein 1NF-E2-Related Factor 2

Identifiers

PMID27814396
PMCPMC5096693
OpenAlexW2548093197

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.