Evidence map›Paper›PMID 27175969›Full record

ArticleEndocrinology2016

High-Fat Diet Promotion of Endometriosis in an Immunocompetent Mouse Model is Associated With Altered Peripheral and Ectopic Lesion Redox and Inflammatory Status.

Melissa E Heard, Stepan B Melnyk, Frank A Simmen, Yanqing Yang, John Mark P Pabona, Rosalia C M Simmen

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 4 pooled it
3.5field-weighted citation impact, top 8% 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

40 citing papers in PubMed, 4 syntheses or guidelines pooled it, 74 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. The interplay between endometriosis and obesity.Trends in endocrinology and metabolism: TEM · 2025
    Review
  11. Article
  12. Endometriosis and Nutrition: Therapeutic Perspectives.Journal of clinical medicine · 2025
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

6 authors at 2 institutions in 2 countries.

Melissa E HeardDepartments of Physiology and Biophysics (M.E.H., F.A.S., Y.Y., J.M.P.P., R.C.M.S.) and Pediatrics (S.B.M.) and Arkansas Children's Hospital Research Institute (S.B.M.), University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205; and Department of Obstetrics and Gynecology (Y.Y.), The Aerospace Central Hospital, Beijing 100049, China.
Stepan B MelnykDepartments of Physiology and Biophysics (M.E.H., F.A.S., Y.Y., J.M.P.P., R.C.M.S.) and Pediatrics (S.B.M.) and Arkansas Children's Hospital Research Institute (S.B.M.), University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205; and Department of Obstetrics and Gynecology (Y.Y.), The Aerospace Central Hospital, Beijing 100049, China.
Frank A SimmenDepartments of Physiology and Biophysics (M.E.H., F.A.S., Y.Y., J.M.P.P., R.C.M.S.) and Pediatrics (S.B.M.) and Arkansas Children's Hospital Research Institute (S.B.M.), University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205; and Department of Obstetrics and Gynecology (Y.Y.), The Aerospace Central Hospital, Beijing 100049, China.
Yanqing YangDepartments of Physiology and Biophysics (M.E.H., F.A.S., Y.Y., J.M.P.P., R.C.M.S.) and Pediatrics (S.B.M.) and Arkansas Children's Hospital Research Institute (S.B.M.), University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205; and Department of Obstetrics and Gynecology (Y.Y.), The Aerospace Central Hospital, Beijing 100049, China.
John Mark P PabonaDepartments of Physiology and Biophysics (M.E.H., F.A.S., Y.Y., J.M.P.P., R.C.M.S.) and Pediatrics (S.B.M.) and Arkansas Children's Hospital Research Institute (S.B.M.), University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205; and Department of Obstetrics and Gynecology (Y.Y.), The Aerospace Central Hospital, Beijing 100049, China.
Rosalia C M SimmenDepartments of Physiology and Biophysics (M.E.H., F.A.S., Y.Y., J.M.P.P., R.C.M.S.) and Pediatrics (S.B.M.) and Arkansas Children's Hospital Research Institute (S.B.M.), University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205; and Department of Obstetrics and Gynecology (Y.Y.), The Aerospace Central Hospital, Beijing 100049, China.
University of Arkansas for Medical Sciences · USAerospace Center Hospital · CN

Funding

CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR029884 · NCRR · UNIV OF ARKANSAS FOR MED SCIS · PI LOWERY, CURTIS L · 2009 to 2011
$11.4M
Arkansas Center for Clinical and Translational ResearchUL1TR000039 · NCATS · UNIV OF ARKANSAS FOR MED SCIS · PI BECK, CORNELIA MARIE, JAMES, LAURA P · 2012 to 2014
$10.0M
UTEROFERRIN GENE EXPRESSION DURING DEVELOPMENTR01HD021961 · NICHD · UNIVERSITY OF FLORIDA · PI SIMMEN, ROSALIA C · 1991 to 2008
$2.1M
Dietary Factors in Colon Cancer PreventionR01CA136493 · NCI · UNIV OF ARKANSAS FOR MED SCIS · PI SIMMEN, FRANK ALBERT · 2010 to 2014
$1.4M
NCATS NIH HHS UL1 TR000039NCI NIH HHS R01 CA136493NCRR NIH HHS UL1 RR029884NICHD NIH HHS R01 HD021961
6 · The paper itself

Abstract

Endometriosis is a benign gynecological condition that causes considerable morbidity due to associated infertility, debilitating pelvic pain and inflammatory dysfunctions. Diet is a highly modifiable risk factor for many chronic diseases, but its contribution to endometriosis has not been extensively investigated, due partly to the paradoxical inverse association between obesity and disease incidence. Nevertheless, chronic exposure to dietary high-fat intake has been linked to greater systemic inflammation and oxidative stress, both features of women with endometriosis. Here, we evaluated the effects of a high-fat diet (HFD) (45% fat kcal) on endometriosis progression using an immunocompetent mouse model where ectopic lesion incidence was induced in wild-type recipients by ip administration of endometrial fragments from transcription factor Krüppel-like factor 9-null donor mice. We show that HFD significantly increased ectopic lesion numbers in recipient mice with no significant weight gain and modifications in systemic ovarian steroid hormone and insulin levels, relative to control diet-fed (17% fat kcal) mice. HFD promotion of lesion establishment was associated with reductions in stromal estrogen receptor 1 isoform and progesterone receptor expression, increased F4/80-positive macrophage infiltration, higher stromal but not glandular epithelial proliferation, and enhanced expression of proinflammatory and prooxidative stress pathway genes. Lesion-bearing HFD-fed mice also displayed higher peritoneal fluid TNFα and elevated local and systemic redox status than control diet-fed counterparts. Our results suggest that HFD intake exacerbates endometriosis outcome in the absence of ovarian dysfunction and insulin resistance in mice and warrants further consideration with respect to clinical management of endometriosis progression and recurrence in nonobese patients.

Indexed as

Diet, High-FatAnimalsApoptosisCell ProliferationDisease Models, AnimalDisease ProgressionEndometriosisFemaleInflammationInsulin ResistanceMiceOxidation-Reduction

Identifiers

PMID27175969
PMCPMC4929556
OpenAlexW2365656613

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.