Evidence map›Paper›PMID 33065227›Full record

ArticleExperimental gerontology2020

17α-Estradiol prevents ovariectomy-mediated obesity and bone loss.

Shivani N Mann, Kevin S Pitel, Molly H Nelson-Holte, Urszula T Iwaniec, Russell T Turner, Roshini Sathiaseelan, James L Kirkland, Augusto Schneider, Katherine T Morris, Subramaniam Malayannan and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Experimental gerontology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

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

12 authors at 4 institutions in 2 countries.

Shivani N MannDepartment of Nutritional Sciences, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA; Oklahoma Center for Geroscience, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA; Harold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. Electronic address: shivani-mann@ouhsc.edu.
Kevin S PitelDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN, USA. Electronic address: pitel.kevin@mayo.edu.
Molly H Nelson-HolteDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN, USA. Electronic address: NelsonHolte.Molly@mayo.edu.
Urszula T IwaniecSchool of Biological and Population Health Sciences, Oregon State University, Corvallis, OR, USA. Electronic address: Urszula.Iwaniec@oregonstate.edu.
Russell T TurnerSchool of Biological and Population Health Sciences, Oregon State University, Corvallis, OR, USA. Electronic address: Russell.Turner@oregonstate.edu.
Roshini SathiaseelanDepartment of Nutritional Sciences, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. Electronic address: Roshini-sathiaseelan@ouhsc.edu.
James L KirklandRobert and Arlene Kogod Center on Aging, Rochester, MN, USA. Electronic address: Kirkland.James@mayo.edu.
Augusto SchneiderFaculdade de Nutrição, Universidade Federal de Pelotas, Pelotas, RS, Brazil. Electronic address: augusto.schneider@ufpel.edu.br.
Katherine T MorrisDepartment of Surgery, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. Electronic address: katherine-morris@ouhsc.edu.
Subramaniam MalayannanDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN, USA. Electronic address: Subramaniam.Malayannan@mayo.edu.
John R HawseDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN, USA. Electronic address: Hawse.John@mayo.edu.
Michael B StoutDepartment of Nutritional Sciences, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA; Oklahoma Center for Geroscience, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA; Harold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. Electronic address: michael-stout@ouhsc.edu.
Mayo Clinic in Arizona · USUniversity of Oklahoma Health Sciences Center · USOregon State University · USUniversidade Federal de Pelotas · BR

Funding

GEROSCIENCE TRAINING PROGRAM IN OKLAHOMAT32AG052363 · NIA · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI Benjamin Francis Miller, William Edmund Sonntag · 2017 to 2026
$3.6M
Cellular senescence and epigenomic remodeling in ovarian agingR01AG069742 · NIA · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI STOUT, MICHAEL B · 2020 to 2024
$2.0M
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
NIA NIH HHS R00 AG051661NIA NIH HHS R01 AG069742NIA NIH HHS T32 AG052363
6 · The paper itself

Abstract

Menopause is a natural physiological process in older women that is associated with reduced estrogen production and results in increased risk for obesity, diabetes, and osteoporosis. 17α-estradiol (17α-E2) treatment in males, but not females, reverses several metabolic conditions associated with advancing age, highlighting sexually dimorphic actions on age-related pathologies. In this study we sought to determine if 17α-E2 could prevent ovariectomy (OVX)-mediated detriments on adiposity and bone parameters in females. Eight-week-old female C57BL/6J mice were subjected to SHAM or OVX surgery and received dietary 17α-E2 during a six-week intervention period. We observed that 17α-E2 prevented OVX-induced increases in body weight and adiposity. Similarly, uterine weight and luminal cell thickness were decreased by OVX and prevented by 17α-E2 treatment. Interestingly, 17α-E2 prevented OVX-induced declines in tibial metaphysis cancellous bone. And similarly, 17α-E2 improved bone density parameters in both tibia and femur cancellous bone, primarily in OVX mice. In contrast, to the effects on cancellous bone, cortical bone parameters were largely unaffected by OVX or 17α-E2. In the non-weight bearing lumbar vertebrae, OVX reduced trabecular thickness but not spacing, while 17α-E2 increased trabecular thickness and reduced spacing. Despite this, 17α-E2 did improve bone volume/tissue volume in lumbar vertebrae. Overall, we found that 17α-E2 prevented OVX-induced increases in adiposity and changes in bone mass and architecture, with minimal effects in SHAM-operated mice. We also observed that 17α-E2 rescued uterine tissue mass and lining morphology to control levels without inducing hypertrophy, suggesting that 17α-E2 could be considered as an adjunct to traditional hormone replacement therapies.

Indexed as

Bone DensityEstradiolAgedAnimalsEstrogensFemaleHumansMiceMice, Inbred C57BLObesityOrgan SizeOvariectomyRatsRats, Sprague-DawleyEstradiolEstrogens17α-EstradiolAdiposityCortical boneOvariectomyTrabecular boneUterus

Identifiers

PMID33065227
PMCPMC8351143
OpenAlexW3093285357

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.