Research ArticleMetabolic Disease

Preclinical efficacy of the GPER-selective agonist G-1 in mouse models of obesity and diabetes

See allHide authors and affiliations

Science Translational Medicine  29 Jan 2020:
Vol. 12, Issue 528, eaau5956
DOI: 10.1126/scitranslmed.aau5956

eLetters is an online forum for ongoing peer review. Submission of eLetters are open to all. Please read our Terms of Service before submitting your own eLetter.

Compose eLetter

Plain text

  • Plain text
    No HTML tags allowed.
  • Web page addresses and e-mail addresses turn into links automatically.
  • Lines and paragraphs break automatically.
Author Information
First or given name, e.g. 'Peter'.
Your last, or family, name, e.g. 'MacMoody'.
Your email address, e.g. higgs-boson@gmail.com
Your role and/or occupation, e.g. 'Orthopedic Surgeon'.
Your organization or institution (if applicable), e.g. 'Royal Free Hospital'.
Statement of Competing Interests
CAPTCHA

This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.

Vertical Tabs

  • RE: Sharma, et al., may be Explained by Dehydroepiandrosterone (DHEA) Levels

    I suggest an alternative explanation of GPER stimulated activity is dehydroepiandrosterone (DHEA). A connection of DHEA and GPER has been established: "Dehydroepiandrosterone Activation of G-protein-coupled Estrogen Receptor Rapidly Stimulates MicroRNA-21 Transcription in Human Hepatocellular Carcinoma Cells," (J Biol Chem. 2015 Jun 19;290(25):15799-811.).

    The multiple disease ameliorative effect you reported about G-1 attracted my attention because I immediately though of DHEA. It is my hypothesis that evolution selected dehydroepiandrosterone (DHEA) because it optimizes replication and transcription of DNA, that is, genes. Therefore, DHEA levels affect all tissues and all tissues compete for available DHEA, especially the brain. (I think evolutionary selection of DHEA produced Mammalia. "Hormones in Mammalian Evolution," Rivista di Biologia / Biology Forum 2001; 94: 177-184, http://anthropogeny.com/Hormones%20in%20Mammalian%20Evolution.htm ). DHEA naturally begins to decline around the ages of twenty to twenty-five, reaching very low levels in old age. When DHEA is low, or decreasing, genes and tissues are adversely affected according to competition for DHEA resulting in disturbances of gene functions; when DHEA is too low, death occurs.

    Also, it is my hypothesis that the hormones estradiol and testosterone, via their stimulated receptors, exert their...

    Show More
    Competing Interests: None declared.

Stay Connected to Science Translational Medicine