Evidence map›Paper›PMID 21386058›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2011

High-fat diet induces an initial adaptation of mitochondrial bioenergetics in the kidney despite evident oxidative stress and mitochondrial ROS production.

Christine Ruggiero, Marilyn Ehrenshaft, Ellen Cleland, Krisztian Stadler

Abstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

68 citing papers in PubMed, 121 citations in OpenAlex.

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  14. Role of miR-379 in high-fat diet-induced kidney injury and dysfunction.American journal of physiology. Renal physiology · 2022
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8 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

Christine RuggieroOxidative Stress and Disease Laboratory, Pennington Biomedical Research Center, Baton Rouge, LA 70808, USA.
Marilyn Ehrenshaft
Ellen Cleland
Krisztian Stadler
Pennington Biomedical Research Center · USNational Institute of Environmental Health Sciences · US

Funding

Research BaseP30DK072476 · NIDDK · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI ROBERT A KESTERSON · 2005 to 2026
$26.5M
THE ROLE OF PROTEIN MALNUTRITION ON CIRCADIAN PHYSIOLOGY OF C57BL/6J MOUSE DAMSP20RR021945 · NCRR · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI GETTYS, THOMAS W · 2006 to 2011
$9.5M
Lipid peroxidation-induced chemical modifications of insulin signaling proteinsR00DK083615 · NIDDK · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI STADLER, KRISZTIAN · 2010 to 2012
$742k
NCRR NIH HHS NIH P20 RR-021945NIDDK NIH HHS DK-083615NIDDK NIH HHS NIH 1P30 DK-072476NIDDK NIH HHS P30 DK072476
6 · The paper itself

Abstract

Obesity and metabolic syndrome are associated with an increased risk for several diabetic complications, including diabetic nephropathy and chronic kidney diseases. Oxidative stress and mitochondrial dysfunction are often proposed mechanisms in various organs in obesity models, but limited data are available on the kidney. Here, we fed a lard-based high-fat diet to mice to investigate structural changes, cellular and subcellular oxidative stress and redox status, and mitochondrial biogenesis and function in the kidney. The diet induced characteristic changes, including glomerular hypertrophy, fibrosis, and interstitial scarring, which were accompanied by a proinflammatory transition. We demonstrate evidence for oxidative stress in the kidney through 3-nitrotyrosine and protein radical formation on high-fat diet with a contribution from iNOS and NOX-4 as well as increased generation of mitochondrial oxidants on carbohydrate- and lipid-based substrates. The increased H(2)O(2) emission in the mitochondria suggests altered redox balance and mitochondrial ROS generation, contributing to the overall oxidative stress. No major derailments were observed in respiratory function or biogenesis, indicating preserved and initially improved bioenergetic parameters and energy production. We suggest that, regardless of the oxidative stress events, the kidney developed an adaptation to maintain normal respiratory function as a possible response to an increased lipid overload. These findings provide new insights into the complex role of oxidative stress and mitochondrial redox status in the pathogenesis of the kidney in obesity and indicate that early oxidative stress-related changes, but not mitochondrial bioenergetic dysfunction, may contribute to the pathogenesis and development of obesity-linked chronic kidney diseases.

Indexed as

DietAdaptation, PhysiologicalAnimalsDietary FatsEnergy IntakeEnergy MetabolismFree RadicalsHydrogen PeroxideImmunohistochemistryInflammationKidneyKidney GlomerulusMaleMiceMice, Inbred C57BLMicroscopy, Confocal3-nitrotyrosineDietary FatsFree RadicalsHydrogen PeroxideNADPH Oxidase 4NADPH OxidasesNitric Oxide Synthase Type IINox4 protein, mouseReactive Oxygen SpeciesSuperoxide DismutaseTyrosine

Identifiers

PMID21386058
PMCPMC3118596
OpenAlexW2150230666

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.