Evidence map›Paper›PMID 29224098›Full record

ReviewAdvances in experimental medicine and biology2017

Role of Estrogens in the Regulation of Liver Lipid Metabolism.

Brian T Palmisano, Lin Zhu, John M Stafford

Registry-linked trialAbstract readReview
In one paragraph

Review in Advances in experimental medicine and biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06523530 (Effect of the Pharmacological Cessation of Menstruation With a GnRH Analog on Hepatic Steatosis in Women With Endometriosis), which is not on this map. Cited by 293 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
293citing papers in PubMed, 3 pooled it
97.8field-weighted citation impact, top 1% 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.

NCT06523530 phase4active not recruitingnot on this mapstarted 2024, after this paper: background citation

Effect of the Pharmacological Cessation of Menstruation With a GnRH Analog on Hepatic Steatosis in Women With Endometriosis

TypeinterventionalSponsorAristotle University Of ThessalonikiRan2024 to 2027Enrolled62ConditionsMetabolic Dysfunction-Associated Steatotic Liver Disease, Nonalcoholic Fatty Liver, EndometriosisArmsGoserelin Acetate 3.6 mg inj, implant
3 · Its place in the literature

Who cites it

293 citing papers in PubMed, 3 syntheses or guidelines pooled it, 495 citations in OpenAlex.

  1. When bad turns good: a systematic review on cholesterol and LDL in longitudinal patient cohorts with Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Pooled it
  2. The Effects of Resveratrol on Menopausal Cardio-metabolic Changes: A Systematic Review.Cardiovascular & hematological disorders drug targets · 2026
    Pooled it
  3. Pooled it
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  14. Sexual dimorphism in the liver.Nature reviews. Gastroenterology & hepatology · 2026
    Review
  15. Article
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  17. The Liver-Testis Axis: Molecular Mechanisms and Clinical Implications.International journal of molecular sciences · 2026
    Review
  18. Article
  19. Article
  20. Article

233 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Brian T PalmisanoTennessee Valley Healthcare System, Veterans Affairs, Nashville, TN, USA.
Lin ZhuTennessee Valley Healthcare System, Veterans Affairs, Nashville, TN, USA.
John M StaffordTennessee Valley Healthcare System, Veterans Affairs, Nashville, TN, USA. john.stafford@vanderbilt.edu.
Vanderbilt University · USVA Tennessee Valley Healthcare System · US

Funding

Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MARY Kay WASHINGTON · 2002 to 2026
$29.9M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007347 · NIGMS · VANDERBILT UNIVERSITY · PI WILLIAMS, CHRISTOPHER S. · 1985 to 2023
$26.3M
Therapeutic Potential of Estrogen-Regulated Metabolism and Cardiovascular RiskR01DK109102 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI STAFFORD, JOHN MICHAEL · 2016 to 2024
$3.6M
The Mechanism of Cetp-Mediated Protection from High-Fat Diet-Induced Insulin ResistanceF30DK104514 · NIDDK · VANDERBILT UNIVERSITY · PI PALMISANO, BRIAN T. · 2014 to 2017
$151k
Cholesteryl ester transfer protein, a novel mediator of insulin sensitivityI01BX002223 · VA · VETERANS HEALTH ADMINISTRATION · PI STAFFORD, JOHN MICHAEL · 2014 to 2017
–
BLRD VA I01 BX002223NIDDK NIH HHS F30 DK104514NIDDK NIH HHS P30 DK058404NIDDK NIH HHS R01 DK109102NIGMS NIH HHS T32 GM007347
6 · The paper itself

Abstract

Before menopause, women are protected from atherosclerotic heart disease associated with obesity relative to men. Sex hormones have been proposed as a mechanism that differentiates this risk. In this review, we discuss the literature around how the endogenous sex hormones and hormone treatment approaches after menopause regulate fatty acid, triglyceride, and cholesterol metabolism to influence cardiovascular risk.The important regulatory functions of estrogen signaling pathways with regard to lipid metabolism have been in part obscured by clinical trials with hormone treatment of women after menopause, due to different formulations, routes of delivery, and pairings with progestins. Oral hormone treatment with several estrogen preparations increases VLDL triglyceride production. Progestins oppose this effect by stimulating VLDL clearance in both humans and animals. Transdermal estradiol preparations do not increase VLDL production or serum triglycerides.Many aspects of sex differences in atherosclerotic heart disease risk are influenced by the distributed actions of estrogens in the muscle, adipose, and liver. In humans, 17β-estradiol (E2) is the predominant circulating estrogen and signals through estrogen receptor alpha (ERα), estrogen receptor beta (ERβ), and G-protein-coupled estrogen receptor (GPER). Over 1000 human liver genes display a sex bias in their expression, and the top biological pathways are in lipid metabolism and genes related to cardiovascular disease. Many of these genes display variation depending on estrus cycling in the mouse. Future directions will likely rely on targeting estrogens to specific tissues or specific aspects of the signaling pathways in order to recapitulate the protective physiology of premenopause therapeutically after menopause.

Indexed as

Lipid MetabolismAnimalsCardiovascular DiseasesEstrogen Receptor alphaEstrogen Replacement TherapyEstrogensFemaleHumansInsulin ResistanceLiverMaleMenopauseMiceModels, AnimalNon-alcoholic Fatty Liver DiseaseProtective FactorsESR1 protein, humanEstrogen Receptor alphaEstrogens

Identifiers

PMID29224098
PMCPMC5763482
OpenAlexW2774259180

What OpenQuestion holds

Textmetadata
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Read underepoch 390

Registered trials

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.