Evidence map›Paper›PMID 26583035›Full record

ArticleNutrition & metabolism2015

FXR expression is associated with dysregulated glucose and lipid levels in the offspring kidney induced by maternal obesity.

Sarah J Glastras, Muh Geot Wong, Hui Chen, Jie Zhang, Amgad Zaky, Carol A Pollock, Sonia Saad

Open access · goldAbstract read
In one paragraph

Article in Nutrition & metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.5field-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

17 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Role of FXR in Renal Physiology and Kidney Diseases.International journal of molecular sciences · 2023
    Review
  7. Drug metabolism and disposition: the biological fate of chemicals · 2022
    Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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 1 country.

Sarah J GlastrasKolling Institute, Department of Medicine, University of Sydney, Sydney, Australia ; Department of Endocrinology, Diabetes and Metabolism, Royal North Shore Hospital, St Leonards, Australia.
Muh Geot WongKolling Institute, Department of Medicine, University of Sydney, Sydney, Australia.
Hui ChenSchool of Life Sciences, Faculty of Science, University of Technology Sydney, Sydney, Australia.
Jie ZhangKolling Institute, Department of Medicine, University of Sydney, Sydney, Australia.
Amgad ZakyKolling Institute, Department of Medicine, University of Sydney, Sydney, Australia.
Carol A PollockKolling Institute, Department of Medicine, University of Sydney, Sydney, Australia.
Sonia SaadKolling Institute, Department of Medicine, University of Sydney, Sydney, Australia.
University of Sydney · AUUniversity of Technology Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMaternal obesity is associated with dysregulation of glucose and lipid metabolism with consequent exposure of the fetus to an abnormal metabolic milieu. It is recognized that maternal obesity predisposes offspring to chronic kidney disease (CKD). We aimed to determine whether the nuclear Farnesoid X receptor (FXR), known to play a role in maintaining homeostasis of glucose and lipid metabolism, is involved in renal injury in offspring of obese mothers.

methodsMaternal obesity was established in a rat model by feeding dams with high-fat diet prior to and during pregnancy and lactation. The offspring's kidneys were examined at postnatal Day 1and Day 20. Human kidney 2 (HK2) cells were exposed to high glucose with or without the FXR agonist GW4064 or when FXR mRNA was silenced.

resultsGlucose intolerance in the offspring of obese mothers was evident at weaning, with associated downregulation of renal FXR expression and upregulation of monocyte chemoattractant protein-1 (MCP-1) and transforming growth factor-β1 (TGF-β1). HK2 cells exposed to high glucose had reduced FXR expression and increased MCP-1, TGF-β1, fibronectin and collagen IV expression, which was reversed in the presence of GW4064. FXR-silenced HK2 cells had amplified pro-inflammatory and pro-fibrotic markers under high glucose conditions.

conclusionsMaternal obesity influences renal expression of pro-inflammatory and fibrotic factors that predispose the offspring to CKD. This was associated with the downregulation of the renal FXR expression suggesting a potential protective role for FXR.

Indexed as

Chronic kidney diseaseDevelopmental programmingFarnesoid X receptorMaternal obesityNuclear hormone receptorRenal injury

Identifiers

PMID26583035
PMCPMC4650952
OpenAlexW2173796941

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.