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Biomedicines
Special Issues
Glucocorticoid Receptor Function in Metabolic Diseases
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Glucocorticoid Receptor Function in Metabolic Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (30 November 2020) | Viewed by 5684

Special Issue Editors

Dr. Jason Collier

E-Mail Website
Guest Editor
Pennington Biomedical Research Center, Baton Rouge, LA, USA
Interests: diabetes; glucocorticoid; insulin resistance; inflammation; metabolic flexibility; obesity; transcription
Special Issues, Collections and Topics in MDPI journals
Dr. Robert Noland

E-Mail Website
Co-Guest Editor
Pennington Biomedical Research Center, Baton Rouge, United States
Interests: diabetes; glucocorticoid; insulin resistance; lipid overload; metabolic flexibility; obesity; substrate oxidation

Special Issue Information

Dear Colleagues,

Glucocorticoids are adrenal-derived hormones that provide important health functions, including serving as outstanding anti-inflammatory molecules. However, when overproduced or used chronically, they also promote a number of deleterious changes to metabolic homeostasis, including losses in lean mass, gain of fat mass, insulin resistance, and high risk of diabetes. Animal studies and clinical data have demonstrated the wide-reaching actions of glucocorticoids within various tissues that impact tissue function and overall health. Delineating the nuances that allow for therapeutic use of glucocorticoids for disease prevention and/or treatment versus those that lead to development of metabolic disease requires greater understanding of glucocorticoid and glucocorticoid receptor biology. In this Special Issue, Glucocorticoid Receptor Function in Metabolic Disease, we call for original papers and leading edge reviews addressing all aspects of glucocorticoid receptor (GR) signaling that will provide deeper insights into metabolic disease. Manuscripts that deal with novel glucocorticoid receptor agonists or studies of existing molecules that impact glucose and lipid homeostasis, insulin resistance, and hyperglycemia by modulating GR activity are welcome. Finally, studies that demonstrate mechanisms of glucocorticoid action that contribute to anti-inflammatory actions as well as metabolic dysfunction are encouraged.

Dr. Jason Collier
Dr. Robert Noland
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Body composition
  • Diabetes
  • Glucocorticoid
  • Glucocorticoid receptor
  • Inflammation
  • Insulin resistance
  • Metabolic flexibility
  • Metabolomics
  • Transcriptomics

Published Papers (2 papers)

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Research

13 pages, 3252 KiB  
Article
The Ubiquitin Ligase SIAH2 Negatively Regulates Glucocorticoid Receptor Activity and Abundance
by Susan J. Burke, Jessica L. Taylor, Heidi M. Batdorf, Robert C. Noland, David H. Burk, Yongmei Yu, Z. Elizabeth Floyd and J. Jason Collier
Biomedicines 2021, 9(1), 22; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9010022 - 30 Dec 2020
Cited by 2 | Viewed by 2045
Abstract
Glucocorticoids are clinically essential drugs used routinely to control inflammation. However, a host of metabolic side effects manifests upon usage beyond a few days. In the present study, we tested the hypothesis that seven-in-absentia mammalian homolog-2 (SIAH2), a ubiquitin ligase that regulates adipogenesis, [...] Read more.
Glucocorticoids are clinically essential drugs used routinely to control inflammation. However, a host of metabolic side effects manifests upon usage beyond a few days. In the present study, we tested the hypothesis that seven-in-absentia mammalian homolog-2 (SIAH2), a ubiquitin ligase that regulates adipogenesis, is important for controlling adipocyte size, inflammation, and the ability of adipose tissue to expand in response to a glucocorticoid challenge. Using mice with global deletion of SIAH2 exposed or not to corticosterone, we found that adipocytes are larger in response to glucocorticoids in the absence of SIAH2. In addition, SIAH2 regulates glucocorticoid receptor (GR) transcriptional activity and total GR protein abundance. Moreover, these studies reveal that there is an increased expression of genes involved in fibrosis and inflammatory signaling pathways found in white adipose tissue in response to glucocorticoids in the absence of SIAH2. In summary, this is the first study to identify a role for SIAH2 to regulate transcriptional activity and abundance of the GR, which leads to alterations in adipose tissue size and gene expression during in vivo exposure to glucocorticoids. Full article
(This article belongs to the Special Issue Glucocorticoid Receptor Function in Metabolic Diseases)
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13 pages, 1689 KiB  
Article
Obesity Augments Glucocorticoid-Dependent Muscle Atrophy in Male C57BL/6J Mice
by Laura C. Gunder, Innocence Harvey, JeAnna R. Redd, Carol S. Davis, Ayat AL-Tamimi, Susan V. Brooks and Dave Bridges
Biomedicines 2020, 8(10), 420; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines8100420 - 15 Oct 2020
Cited by 8 | Viewed by 3161
Abstract
Glucocorticoids promote muscle atrophy by inducing a class of proteins called atrogenes, resulting in reductions in muscle size and strength. In this work, we evaluated whether a mouse model with pre-existing diet-induced obesity had altered glucocorticoid responsiveness. We observed that all animals treated [...] Read more.
Glucocorticoids promote muscle atrophy by inducing a class of proteins called atrogenes, resulting in reductions in muscle size and strength. In this work, we evaluated whether a mouse model with pre-existing diet-induced obesity had altered glucocorticoid responsiveness. We observed that all animals treated with the synthetic glucocorticoid dexamethasone had reduced strength, but that obesity exacerbated this effect. These changes were concordant with more pronounced reductions in muscle size, particularly in Type II muscle fibers, and potentiated induction of atrogene expression in the obese mice relative to lean mice. Furthermore, we show that the reductions in lean mass do not fully account for the dexamethasone-induced insulin resistance observed in these mice. Together, these data suggest that obesity potentiates glucocorticoid-induced muscle atrophy. Full article
(This article belongs to the Special Issue Glucocorticoid Receptor Function in Metabolic Diseases)
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