Evidence map›Paper›PMID 23233541›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2013

NOX2 deficiency attenuates markers of adiposopathy and brain injury induced by high-fat diet.

Jennifer K Pepping, Linnea R Freeman, Sunita Gupta, Jeffrey N Keller, Annadora J Bruce-Keller

Abstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

57 citing papers in PubMed, 95 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Cross-Talk of NADPH Oxidases and Inflammation in Obesity.Antioxidants (Basel, Switzerland) · 2023
    Review
  11. NOX Dependent ROS Generation and Cell Metabolism.International journal of molecular sciences · 2023
    Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Cognitive impairment in obese rat model: role of glial cells.International journal of obesity (2005) · 2021
    Article
  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

5 authors at 2 institutions in 1 country.

Jennifer K PeppingPennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA 70808, USA.
Linnea R Freeman
Sunita Gupta
Jeffrey N Keller
Annadora J Bruce-Keller
Pennington Biomedical Research Center · USLouisiana State University System · US

Funding

Research BaseP30DK072476 · NIDDK · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI Peter Todd Katzmarzyk · 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
NCRR NIH HHS P20 RR-021945NIA NIH HHS AG-05119NIDDK NIH HHS P30 DK-072476NIDDK NIH HHS P30 DK072476
6 · The paper itself

Abstract

The consumption of high-fat/calorie diets in modern societies is likely a major contributor to the obesity epidemic, which can increase the prevalence of cancer, cardiovascular disease, and neurological impairment. Obesity may precipitate decline via inflammatory and oxidative signaling, and one factor linking inflammation to oxidative stress is the proinflammatory, pro-oxidant enzyme NADPH oxidase. To reveal the role of NADPH oxidase in the metabolic and neurological consequences of obesity, the effects of high-fat diet were compared in wild-type C57Bl/6 (WT) mice and in mice deficient in the NAPDH oxidase subunit NOX2 (NOX2KO). While diet-induced weight gains in WT and NOX2KO mice were similar, NOX2KO mice had smaller visceral adipose deposits, attenuated visceral adipocyte hypertrophy, and diminished visceral adipose macrophage infiltration. Moreover, the detrimental effects of HFD on markers of adipocyte function and injury were attenuated in NOX2KO mice; NOX2KO mice had improved glucose regulation, and evaluation of NOX2 expression identified macrophages as the primary population of NOX2-positive cells in visceral adipose. Finally, brain injury was assessed using markers of cerebrovascular integrity, synaptic density, and reactive gliosis, and data show that high-fat diet disrupted marker expression in WT but not NOX2KO mice. Collectively, these data indicate that NOX2 is a significant contributor to the pathogenic effects of high-fat diet and reinforce a key role for visceral adipose inflammation in metabolic and neurological decline. Development of NOX-based therapies could accordingly preserve metabolic and neurological function in the context of metabolic syndrome.

Indexed as

AdiposityAnimalsBiomarkersBrainDiet, High-FatHypertrophyIntra-Abdominal FatMacrophagesMaleMembrane GlycoproteinsMetabolic SyndromeMiceMice, Inbred C57BLMice, KnockoutNADPH Oxidase 2NADPH OxidasesBiomarkersCybb protein, mouseMembrane GlycoproteinsNADPH Oxidase 2NADPH OxidasesNerve Tissue ProteinsProtein Subunits

Identifiers

PMID23233541
PMCPMC3566505
OpenAlexW2145683389

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.