Evidence map›Paper›PMID 22422828›Full record

ArticleDisease models & mechanisms2012

High-fat-diet-induced obesity causes an inflammatory and tumor-promoting microenvironment in the rat kidney.

Kerstin Stemmer, Diego Perez-Tilve, Gayathri Ananthakrishnan, Anja Bort, Randy J Seeley, Matthias H Tschöp, Daniel R Dietrich, Paul T Pfluger

Open access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.2field-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

39 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. N-methyl-D-aspartate receptor inhibition protects against obesity-induced kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2026
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  12. Role of microRNAs in Obesity-Related Kidney Disease.International journal of molecular sciences · 2021
    Review
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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

8 authors at 3 institutions in 2 countries.

Kerstin StemmerDepartment of Internal Medicine, Metabolic Diseases Institute, University of Cincinnati, Division of Endocrinology and Metabolism, 2170 East Galbraith Road, Building E, Cincinnati, OH 45237, USA. kerstin.stemmer@helmholtz-muenchen.de
Diego Perez-Tilve
Gayathri Ananthakrishnan
Anja Bort
Randy J Seeley
Matthias H Tschöp
Daniel R Dietrich
Paul T Pfluger
University of Cincinnati · USHelmholtz Zentrum München · DEUniversity of Konstanz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity and concomitant comorbidities have emerged as public health problems of the first order. For instance, obese individuals have an increased risk for kidney cancer. However, direct mechanisms linking obesity with kidney cancer remain elusive. We hypothesized that diet-induced obesity (DIO) promotes renal carcinogenesis by inducing an inflammatory and tumor-promoting microenvironment. We compared chow-fed lean Wistar rats with those that were sensitive (DIOsens) or partially resistant (DIOres) to DIO to investigate the impact of body adiposity versus dietary nutrient overload in the development of renal preneoplasia and activation of tumor-promoting signaling pathways. Our data clearly show a correlation between body adiposity, the severity of nephropathy, and the total number and incidence of preneoplastic renal lesions. However, similar plasma triglyceride, plasma free fatty acid and renal triglyceride levels were found in chow-fed, DIOres and DIOsens rats, suggesting that lipotoxicity is not a critical contributor to the renal pathology. Obesity-related nephropathy was further associated with regenerative cell proliferation, monocyte infiltration and higher renal expression of monocyte chemotactic protein-1 (MCP-1), interleukin (IL)-6, IL-6 receptor and leptin receptor. Accordingly, we observed increased signal transducer and activator of transcription 3 (STAT3) and mammalian target of rapamycin (mTOR) phosphorylation in tubules with preneoplastic phenotypes. In summary, our results demonstrate that high body adiposity induces an inflammatory and proliferative microenvironment in rat kidneys that promotes the development of preneoplastic lesions, potentially via activation of the STAT3 and mTOR signaling pathways.

Indexed as

Diet, High-FatTumor MicroenvironmentAnimalsCell Transformation, NeoplasticHormonesInflammationKidneyKidney NeoplasmsLipidsMaleObesityPhosphorylationRatsRats, WistarSignal TransductionSTAT3 Transcription FactorHormonesLipidsSTAT3 Transcription FactorTOR Serine-Threonine Kinases

Identifiers

PMID22422828
PMCPMC3424460
OpenAlexW2107925903

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.