Evidence map›Paper›PMID 22209722›Full record

ArticleProstaglandins & other lipid mediators2012

EET agonist prevents adiposity and vascular dysfunction in rats fed a high fat diet via a decrease in Bach 1 and an increase in HO-1 levels.

Komal Sodhi, Nitin Puri, Kazuyoshi Inoue, John R Falck, Michal L Schwartzman, Nader G Abraham

Open access · greenAbstract read
In one paragraph

Article in Prostaglandins & other lipid mediators, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

40 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
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  11. HO-1 overexpression and underexpression: Clinical implications.Archives of biochemistry and biophysics · 2019
    Review
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  17. Epoxide metabolites of arachidonate and docosahexaenoate function conversely in acute kidney injury involved in GSK3β signaling.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
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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

6 authors at 3 institutions in 1 country.

Komal SodhiDepartment of Physiology and Pharmacology, The University of Toledo College of Medicine, Health Education Building, 3000 Arlington Avenue, Toledo, OH 43614-2598, USA.
Nitin Puri
Kazuyoshi Inoue
John R Falck
Michal L Schwartzman
Nader G Abraham
University of Toledo · USNew York Medical College · USThe University of Texas Southwestern Medical Center · US

Funding

Vasoregulatory Function of CYP2E1-Derived EicosanoidsP01HL034300 · NHLBI · NEW YORK MEDICAL COLLEGE · PI SCHWARTZMAN, MICHAL LANIADO · 1985 to 2015
$33.4M
TRANSPORT EFFECTS OF ARACHIDONATE METABOLITES IN PERFUSED TUBULEP01DK038226 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BROWN, NANCY J. · 1986 to 2015
$22.1M
HEME OXYGENASE REGULATION OF EICOSANOID BIOSYNTHESISR01DK056601 · NIDDK · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI ABRAHAM, NADER G. · 2001 to 2013
$4.4M
Oxidative Stress and Vascular HO in DiabetesR01DK068134 · NIDDK · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI ABRAHAM, NADER G. · 2006 to 2010
$1.7M
NHLBI NIH HHS HL34300NHLBI NIH HHS HL55601NHLBI NIH HHS P01 HL034300NIDDK NIH HHS DK068134NIDDK NIH HHS P01 DK038226NIDDK NIH HHS R01 DK056601NIDDK NIH HHS R01 DK068134
6 · The paper itself

Abstract

Recent reports have shown interplay between EETs (epoxides) and the heme oxygenase (HO) system in attenuating adipogenesis in cell culture models; prompting an examination of the effectiveness of EET agonist on obesity and associated cardio-metabolic dysfunction. Patho-physiological effects of an EET agonist (NUDSA) were contrasted in the absence and in the presence of stannous mesoporphyrin (an HO inhibitor) in SD rats fed a high fat (58%, HF) for 16 weeks. Animals on HF diet exhibited enhanced oxidative stress, increased levels of inflammatory cytokines and decreased levels of adiponectin along with reduced vascular and adipose tissue levels of EETs, HO-1; as compared to control rats (11% dietary fat). Treatment with NUDSA not only reversed serum adiponectin and vascular and adipose tissue levels of EETs and HO-1, but also, decreased blood pressure, subcutaneous and visceral fat content and serum TNFα and IL-6 levels in rats on HF diet. Aortic endothelial function, peNOS expression and adipose tissue markers of energy homeostasis i.e. pAMPK, Sirt1 and FAS, impaired in rats fed a HF diet, were restored in animals treated with this EET agonist. That NUDSA enhanced HO-1 expression, was accompanied by increase in p-GSK-3β and pAKT levels along with attenuation of adipose tissue levels of Bach 1--the transcriptional suppresser of HO-1 expression. Prevention of these beneficial effects of NUDSA, in animals on HF diet and concurrently exposed to NUDSA and SnMP, supports the role of EET-HO interaction in mediating such effects. Taken together, our findings suggest that the EETs stimulate HO-1 expression via suppression of Bach 1 and interplay of these two systems affords vascular and metabolic protection in diet induced obesity.

Indexed as

Diet, High-FatAdiponectinAdiposityAnimalsAspartic AcidBasic-Leucine Zipper Transcription FactorsBiomarkersBody WeightCytokinesEicosanoidsEndothelium, VascularFerritinsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHeme Oxygenase (Decyclizing)Homeostasis2-(11-(nonyloxy)undec-8-enamido)succinic acidAdiponectinAspartic AcidBach 1 protein, ratBasic-Leucine Zipper Transcription FactorsBiomarkersCytokinesEicosanoidsFerritinsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, ratHeme Oxygenase (Decyclizing)Hmox1 protein, ratInflammation MediatorsMetalloporphyrinsProto-Oncogene Proteins c-aktRepressor Proteinsstannous mesoporphyrin

Identifiers

PMID22209722
PMCPMC3449325
OpenAlexW2002937742

What OpenQuestion holds

Textmetadata
LicenceTDM
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.