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Title:
GPER/GPR30 Knockout Mice: Effects of GPER on Metabolism | SpringerLink
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Endogenous estrogens, predominantly 17β-estradiol (E2), mediate various diverse effects throughout the body in both normal physiology and disease. Actions include development (including puberty) and reproduction as well as additional effects throughout life in...
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Keywords {🔍}
article, google, scholar, cas, estrogen, prossnitz, gper, receptor, endocrinol, receptors, protocol, rev, mice, proteincoupled, insulin, diabetes, privacy, cookies, content, information, publish, effects, metabolism, sharma, disease, metabolic, obesity, glucose, chapter, nat, barton, mol, search, gpergpr, knockout, regulation, oestrogen, clegg, endocrinology, biol, download, springer, usd, function, personal, data, log, journal, research, eric,
Topics {✒️}
protein-coupled estrogen receptor protein-coupled receptor homolog gper/gpr30 knockout mice month download article/chapter estradiol-induced insulin secretion privacy choices/manage cookies murine genetic knockout estrogen-induced activation beta-cell dysfunction unm cancer center insulin tolerance tests male mice results gper/gpr30 antagonist predominantly 17β-estradiol device instant download pancreatic beta-cells estrogen receptors sex steroid action reduces bone growth gper ko mice knockout mice european economic area frackelton ar jr biomolecular screening converge increases blood pressure nih grants ca116662 editor information editors estrogen signaling gper-selective ligands journal finder publish conditions privacy policy protocol sharma accepting optional cookies actions include development body fat distribution mauvais-jarvis filardo ej revankar cm author information authors human visceral obesity protocol usd 49 main content log protocol cite oestrogen receptors estrogen biology cell metab 14 update article 16 prossnitz er gpr30 antagonist social media
Questions {❓}
- Prossnitz ER, Hathaway HJ (2015) What have we learned about GPER function in physiology and disease from knockout mice?
Schema {🗺️}
ScholarlyArticle:
headline:GPER/GPR30 Knockout Mice: Effects of GPER on Metabolism
pageEnd:502
pageStart:489
image:https://media.springernature.com/w153/springer-static/cover/book/978-1-4939-3127-9.jpg
genre:
Springer Protocols
isPartOf:
name:Estrogen Receptors
isbn:
978-1-4939-3127-9
978-1-4939-3126-2
type:Book
publisher:
name:Springer New York
logo:
url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
type:ImageObject
type:Organization
author:
name:Geetanjali Sharma
affiliation:
name:University of New Mexico Health Sciences Center
address:
name:Department of Internal Medicine and UNM Comprehensive Cancer Center, University of New Mexico Health Sciences Center, Albuquerque, USA
type:PostalAddress
type:Organization
type:Person
name:Eric R. Prossnitz
affiliation:
name:University of New Mexico Health Sciences Center
address:
name:Department of Internal Medicine and UNM Comprehensive Cancer Center, University of New Mexico Health Sciences Center, Albuquerque, USA
type:PostalAddress
type:Organization
email:[email protected]
type:Person
keywords:
Estrogen
,
GPER
,
GPR30
,
Metabolism
,
Obesity
,
Adipose
,
Adipocyte
, Insulin resistance, Insulin sensitivity, Glucose tolerance,
Type 2 diabetes
description:Endogenous estrogens, predominantly 17β-estradiol (E2), mediate various diverse effects throughout the body in both normal physiology and disease. Actions include development (including puberty) and reproduction as well as additional effects throughout life in the metabolic, endocrine, musculoskeletal, nervous, cardiovascular, and immune systems. The actions of E2 have traditionally been attributed to the classical nuclear estrogen receptors (ERα and ERβ) that largely mediate transcriptional/genomic activities. However, more recently the G protein-coupled estrogen receptor GPER/GPR30 has become recognized as an essential mediator of certain, and particularly rapid, signaling events in response to E2. Murine genetic knockout (KO) models represent an important approach to understand the mechanisms of E2 action in physiology and disease. Studies of GPER KO mice over the last years have revealed functions for GPER in the regulation of obesity, insulin resistance and glucose intolerance, among other areas of (patho)physiology. This chapter focuses on methods for the evaluation of metabolic parameters in vivo and ex vivo with an emphasis on glucose homeostasis and metabolism through the use of glucose and insulin tolerance tests, pancreatic islet and adipocyte isolation and characterization.
datePublished:2016
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name:University of New Mexico Health Sciences Center
address:
name:Department of Internal Medicine and UNM Comprehensive Cancer Center, University of New Mexico Health Sciences Center, Albuquerque, USA
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address:
name:Department of Internal Medicine and UNM Comprehensive Cancer Center, University of New Mexico Health Sciences Center, Albuquerque, USA
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name:Department of Internal Medicine and UNM Comprehensive Cancer Center, University of New Mexico Health Sciences Center, Albuquerque, USA
type:PostalAddress
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name:Eric R. Prossnitz
affiliation:
name:University of New Mexico Health Sciences Center
address:
name:Department of Internal Medicine and UNM Comprehensive Cancer Center, University of New Mexico Health Sciences Center, Albuquerque, USA
type:PostalAddress
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email:[email protected]
PostalAddress:
name:Department of Internal Medicine and UNM Comprehensive Cancer Center, University of New Mexico Health Sciences Center, Albuquerque, USA
name:Department of Internal Medicine and UNM Comprehensive Cancer Center, University of New Mexico Health Sciences Center, Albuquerque, USA
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