Evidence map›Paper›PMID 33289482›Full record

ArticleeLife2020

Health benefits attributed to 17α-estradiol, a lifespan-extending compound, are mediated through estrogen receptor α.

Shivani N Mann, Niran Hadad, Molly Nelson Holte, Alicia R Rothman, Roshini Sathiaseelan, Samim Ali Mondal, Martin-Paul Agbaga, Archana Unnikrishnan, Malayannan Subramaniam, John Hawse and 3 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
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  17. A Genetically Heterogeneous Rat Model with Divergent Mitochondrial Genomes.The journals of gerontology. Series A, Biological sciences and medical sciences · 2023
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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

13 authors at 6 institutions in 1 country.

Shivani N MannDepartment of Nutritional Sciences, University of Oklahoma Health Sciences Center, Oklahoma City, United States.
Niran HadadThe Jackson Laboratory, Bar Harbor, United States.
Molly Nelson HolteDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, United States.
Alicia R RothmanDepartment of Nutritional Sciences, University of Oklahoma Health Sciences Center, Oklahoma City, United States.
Roshini SathiaseelanDepartment of Nutritional Sciences, University of Oklahoma Health Sciences Center, Oklahoma City, United States.
Samim Ali MondalDepartment of Nutritional Sciences, University of Oklahoma Health Sciences Center, Oklahoma City, United States.
Martin-Paul AgbagaHarold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, United States.
Archana UnnikrishnanHarold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, United States.
Malayannan SubramaniamDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, United States.
John HawseDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, United States.
Derek M HuffmanDepartment of Molecular Pharmacology, Albert Einstein College of Medicine, New York, United States.
Willard M FreemanOklahoma Center for Geroscience, University of Oklahoma Health Sciences Center, Oklahoma City, United States.ORCID 0000-0001-7027-999X
Michael B StoutDepartment of Nutritional Sciences, University of Oklahoma Health Sciences Center, Oklahoma City, United States.ORCID 0000-0002-9996-9123
University of Oklahoma Health Sciences Center · USMayo Clinic · USAlbert Einstein College of Medicine · USDean McGee Eye Institute · USJackson Laboratory · USOklahoma Medical Research Foundation · US

Funding

Einstein's Nathan Shock Center of Excellence in Basic Biology of AgingP30AG038072 · NIA · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI BARZILAI, NIR J · 2010 to 2024
$10.8M
CORE--MOLECULAR BIOLOGYP30EY012190 · NEI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ANDERSON, ROBERT E · 1999 to 2009
$5.2M
GEROSCIENCE TRAINING PROGRAM IN OKLAHOMAT32AG052363 · NIA · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI Benjamin Francis Miller, William Edmund Sonntag · 2017 to 2026
$3.6M
Sex divergence and cell specificity of age-related hippocampal DNA modificationsR01AG059430 · NIA · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI FREEMAN, WILLARD M · 2019 to 2023
$2.7M
Cellular senescence and epigenomic remodeling in ovarian agingR01AG069742 · NIA · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI STOUT, MICHAEL B · 2020 to 2024
$2.0M
Essential Role of Very Long Chain Fatty Acids in Retinal FunctionR01EY030513 · NEI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI AGBAGA, MARTIN-PAUL · 2019 to 2023
$1.8M
Mechanisms of metabolic, inflammatory and healthspan enhancement by 17a-estradiolR00AG051661 · NIA · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI STOUT, MICHAEL B · 2018 to 2020
$746k
Defining the Mechanism of Altered Very Long Chain Fatty Acid Metabolism in Neuro-Ichthyotic Disorders.R21AR076035 · NIAMS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI AGBAGA, MARTIN-PAUL · 2019 to 2020
$351k
Dynamics of the brain epigenome with agingI01BX003906 · VA · OKLAHOMA CITY VA MEDICAL CENTER · PI FREEMAN, WILLARD M · 2018 to 2021
–
BLRD VA I01 BX003906NEI NIH HHS P30 EY012190NEI NIH HHS R01 EY030513NIAMS NIH HHS R21 AR076035NIA NIH HHS P30 AG038072NIA NIH HHS R00 AG051661NIA NIH HHS R01 AG059430NIA NIH HHS R01 AG069742NIA NIH HHS T32 AG052363NIH HHS R00 AG51661Veterans Affairs Oklahoma City I01BX003906
6 · The paper itself

Abstract

Metabolic dysfunction underlies several chronic diseases, many of which are exacerbated by obesity. Dietary interventions can reverse metabolic declines and slow aging, although compliance issues remain paramount. 17α-estradiol treatment improves metabolic parameters and slows aging in male mice. The mechanisms by which 17α-estradiol elicits these benefits remain unresolved. Herein, we show that 17α-estradiol elicits similar genomic binding and transcriptional activation through estrogen receptor α (ERα) to that of 17β-estradiol. In addition, we show that the ablation of ERα completely attenuates the beneficial metabolic effects of 17α-E2 in male mice. Our findings suggest that 17α-E2 may act through the liver and hypothalamus to improve metabolic parameters in male mice. Lastly, we also determined that 17α-E2 improves metabolic parameters in male rats, thereby proving that the beneficial effects of 17α-E2 are not limited to mice. Collectively, these studies suggest ERα may be a drug target for mitigating chronic diseases in male mammals.

Indexed as

LongevityAnimalsEstradiolEstrogen Receptor alphaFemaleGene Expression RegulationHypothalamusInsulin ResistanceLiverMaleMiceMice, KnockoutRatsEstradiolEstrogen Receptor alpha17α-estradiolagingestrogen receptorhypothalamusmedicinemetabolismmouseobesityrat

Identifiers

PMID33289482
PMCPMC7744101
OpenAlexW3112165855

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.