Evidence map›Paper›PMID 29224106›Full record

ReviewAdvances in experimental medicine and biology2017

G-Protein-Coupled Estrogen Receptor (GPER) and Sex-Specific Metabolic Homeostasis.

Geetanjali Sharma, Eric R Prossnitz

Open access · greenAbstract 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. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
30.8field-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.

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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. An In Vivo Model of Estrogen Supplementation Concerning the Expression of CaJournal of cardiovascular development and disease · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Sexual Dimorphism in Cardiometabolic Diseases: The Role of AMPK.International journal of molecular sciences · 2023
    Review
  17. Article
  18. Review
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Geetanjali SharmaDivision of Molecular Medicine, Department of Internal Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM, USA. gsharma@salud.unm.edu.
Eric R ProssnitzDivision of Molecular Medicine, Department of Internal Medicine, and Autophagy, Inflammation and Metabolism Center of Biomedical Research Excellence, University of New Mexico Health Sciences Center, Albuquerque, NM, USA. eprossnitz@salud.unm.edu.
University of New Mexico · US

Funding

WOMEN'S CANCERS RESEARCH PROGRAMP30CA118100 · NCI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Yolanda Sanchez · 2005 to 2026
$57.1M
Molecular Mechanisms and Applications of Novel ER/GPER-selective LigandsR01CA194496 · NCI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI ARTERBURN, JEFFREY B, PROSSNITZ, ERIC R · 2016 to 2025
$4.1M
G protein-coupled estrogen receptor GPER and breast carcinogenesisR01CA163890 · NCI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI PROSSNITZ, ERIC R · 2012 to 2023
$3.3M
Development of GPR30-Selective LigandsR01CA127731 · NCI · UNIVERSITY OF NEW MEXICO · PI ARTERBURN, JEFFREY B, OPREA, TUDOR I · 2008 to 2012
$1.7M
NCI NIH HHS P30 CA118100NCI NIH HHS R01 CA127731NCI NIH HHS R01 CA163890NCI NIH HHS R01 CA194496
6 · The paper itself

Abstract

Obesity and metabolic syndrome display disparate prevalence and regulation between males and females. Human, as well as rodent, females with regular menstrual/estrous cycles exhibit protection from weight gain and associated chronic diseases. These beneficial effects are predominantly attributed to the female hormone estrogen, specifically 17β-estradiol (E2). E2 exerts its actions via multiple receptors, nuclear and extranuclear estrogen receptor (ER) α and ERβ, and the G-protein-coupled estrogen receptor (GPER, previously termed GPR30). The roles of GPER in metabolic homeostasis are beginning to emerge but are complex and remain unclear. The discovery of GPER-selective pharmacological agents (agonists and antagonists) and the availability of GPER knockout mice have significantly enhanced our understanding of the functions of GPER in normal physiology and disease. GPER action manifests pleiotropic effects in metabolically active tissues such as the pancreas, adipose, liver, and skeletal muscle. Cellular and animal studies have established that GPER is involved in the regulation of body weight, feeding behavior, inflammation, as well as glucose and lipid homeostasis. GPER deficiency leads to increased adiposity, insulin resistance, and metabolic dysfunction in mice. In contrast, pharmacologic stimulation of GPER in vivo limits weight gain and improves metabolic output, revealing a promising novel therapeutic potential for the treatment of obesity and diabetes.

Indexed as

Energy MetabolismAnimalsAnti-Obesity AgentsBody WeightDiabetes MellitusEstrogensFemaleHomeostasisHumansHypoglycemic AgentsMaleObesityPancreasReceptors, EstrogenReceptors, G-Protein-CoupledSex CharacteristicsAnti-Obesity AgentsEstrogensGPER1 protein, humanHypoglycemic AgentsReceptors, EstrogenReceptors, G-Protein-CoupledEstrogenGPERInflammationInsulin resistanceMetabolismObesity

Identifiers

PMID29224106
PMCPMC6656363
OpenAlexW2775249880

What OpenQuestion holds

Textmetadata
LicenceTDM
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.