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We began analyzing https://link.springer.com/protocol/10.1007/978-1-4939-3127-9_38, but it redirected us to https://link.springer.com/protocol/10.1007/978-1-4939-3127-9_38. The analysis below is for the second page.

Title[redir]:
GPER/GPR30 Knockout Mice: Effects of GPER on Metabolism | SpringerLink
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...

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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

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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:
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            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
      isAccessibleForFree:
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Book:
      name:Estrogen Receptors
      isbn:
         978-1-4939-3127-9
         978-1-4939-3126-2
Organization:
      name:Springer New York
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         type:ImageObject
      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
      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
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      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
      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]
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
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

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