Evidence map›Paper›PMID 26571223›Full record

ArticlePediatric research2016

Post-weaning high-fat diet accelerates kidney injury, but not hypertension programmed by maternal diabetes.

Yessoufou Aliou, Min-Chun Liao, Xin-Ping Zhao, Shiao-Ying Chang, Isabelle Chenier, Julie R Ingelfinger, Shao-Ling Zhang

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Pediatric research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
5.2field-weighted citation impact, top 5% 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

13 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. ATDiabetologia · 2021
    Article
  6. Article
  7. Article
  8. PeerJ · 2019
    Article
  9. Article
  10. Proximal Tubular Cannabinoid-1 Receptor Regulates Obesity-Induced CKD.Journal of the American Society of Nephrology : JASN · 2017
    Article
  11. Article
  12. Article
  13. 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

7 authors at 2 institutions in 2 countries.

Yessoufou AliouCentre de recherche du Centre hospitalier de l'Universite de Montreal (CRCHUM), Universite de Montreal, Montréal, Quebec, Canada.
Min-Chun LiaoCentre de recherche du Centre hospitalier de l'Universite de Montreal (CRCHUM), Universite de Montreal, Montréal, Quebec, Canada.
Xin-Ping ZhaoCentre de recherche du Centre hospitalier de l'Universite de Montreal (CRCHUM), Universite de Montreal, Montréal, Quebec, Canada.
Shiao-Ying ChangCentre de recherche du Centre hospitalier de l'Universite de Montreal (CRCHUM), Universite de Montreal, Montréal, Quebec, Canada.
Isabelle ChenierCentre de recherche du Centre hospitalier de l'Universite de Montreal (CRCHUM), Universite de Montreal, Montréal, Quebec, Canada.
Julie R IngelfingerPediatric Nephrology Unit, Massachusetts General Hospital and Harvard Medical School Boston, Boston, Massachusetts.
Shao-Ling ZhangCentre de recherche du Centre hospitalier de l'Universite de Montreal (CRCHUM), Universite de Montreal, Montréal, Quebec, Canada.
Centre Hospitalier de l’Université de Montréal · CAMassachusetts General Hospital · US

Funding

Canadian Institutes of Health Research MOP115025
6 · The paper itself

Abstract

backgroundThe aim of this study was to establish the underlying mechanisms by which a post-weaning high-fat diet (HFD) accelerates the perinatal programming of kidney injury occurring in the offspring of diabetic mothers.

methodsMale mice, offspring of nondiabetic and diabetic dams were fed with normal diet (ND) or HFD from 4 to 20 wk of age. Rat renal proximal tubular cells were used in vitro.

resultsOn ND, the offspring of dams with severe maternal diabetes had an intrauterine growth restriction (IUGR) phenotype and developed mild hypertension and evidence of kidney injury in adulthood. Exposing the IUGR offspring to HFD resulted in rapid weight gain, catch-up growth, and later to profound kidney injury with activation of renal TGFβ1 and collagen type IV expression, increased oxidative stress, and enhanced renal lipid deposition, but not systemic hypertension. Given our data, we speculate that HFD or free fatty acids may accelerate the process of perinatal programming of kidney injury, via increased CD36 and fatty acid-binding protein 4 expression, which may target reactive oxygen species, nuclear factor-kappa B, and TGFβ1 signaling in vivo and in vitro.

conclusionEarly postnatal exposure to overnutrition with a HFD increases the risk of development of kidney injury, but not hypertension, in IUGR offspring of dams with maternal diabetes.

Indexed as

AnimalsApoptosisBody WeightCD36 AntigensDiabetes, GestationalDiet, High-FatFatty Acid-Binding ProteinsFemaleFetal Growth RetardationGlucose Tolerance TestHypertensionKidneyKidney DiseasesKidney TubulesMaleMiceCD36 AntigensFabp4 protein, mouseFatty Acid-Binding Proteins

Identifiers

PMID26571223
OpenAlexW2286331687

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.