Feature Papers in Endocrines: 2024

A special issue of Endocrines (ISSN 2673-396X).

Deadline for manuscript submissions: 1 December 2024 | Viewed by 2038

Special Issue Editors


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Guest Editor
Department of Health Sciences, University “Magna Graecia” of Catanzaro, 88100 Catanzaro, Italy
Interests: pathophysiology of insulin action and insulin signaling; molecular genetics of type 2 diabetes and severe insulin resistance syndromes; gestational diabetes mellitus; pharmacogenetics of type 2 diabetes; obesity, inflammation and cancer; transcriptional regulation of glucose metabolism; mechanisms of gene regulation and transcription networks; pituitary and thyroid tumors; animal models of insulin resistance and type 2 diabetes; diagnostic and prognostic biomarkers and therapeutic targets in diabetes
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Health Sciences, University “Magna Graecia” of Catanzaro, 88100 Catanzaro, Italy
Interests: diabetes; pharmacological therapies for type 2 diabetes; gestational diabetes
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

For this Special Issue, we are interested in high-quality papers published in an open access format, whether submitted by Editorial Board Members or by leading experts invited by the Editorial Office and the Editor-in-Chief. Submissions should be long research papers (or review articles) with full and detailed summaries of the author's own work.

Prof. Dr. Antonio Brunetti
Dr. Maria Mirabelli
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. Endocrines is an international peer-reviewed open access quarterly 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 1000 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

  • obesity, diabetes mellitus and metabolic syndrome
  • lipid metabolism and cardiovascular implications
  • adrenal disorders and electrolyte balance
  • thyroid endocrinology
  • parathyroid disorders, mineral metabolism and bone functions
  • neuroendocrinology and pituitary disorders
  • endocrine oncology
  • andrology and male sexual function
  • female reproductive system and pregnancy endocrinology
  • exercise endocrinology
  • endocrine immunology, cytokines and cell signaling
  • pediatric endocrinology and growth disorders

Published Papers (2 papers)

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Research

20 pages, 3481 KiB  
Article
Male LEW.1WR1 Rats Develop Metabolic Dysfunction, Steatohepatitis, and Liver Damage
by Quiana C. Wilkerson-Vidal, Madushika M. Wimalarathne, Emily C. Hunt, Luis Mercado, Moses Adaji David, Christopher R. Apperson, Alan Smiley, Sharifa Tahirah Love-Rutledge and Bernhard W. G. Vogler
Endocrines 2024, 5(2), 166-185; https://doi.org/10.3390/endocrines5020012 - 19 Apr 2024
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Abstract
Most patients with non-alcoholic steatohepatitis (NASH) have insulin resistance, and there is a near-universal association between NASH and insulin resistance. Insulin resistance induces lipid accumulation in the liver, leading to the development of metabolic syndrome. However, most NASH rodent models fail to develop [...] Read more.
Most patients with non-alcoholic steatohepatitis (NASH) have insulin resistance, and there is a near-universal association between NASH and insulin resistance. Insulin resistance induces lipid accumulation in the liver, leading to the development of metabolic syndrome. However, most NASH rodent models fail to develop metabolic syndrome. LEW.1WR1 rats that are 23 weeks old showed increased body mass, epididymal fat, and liver mass, suggesting obesity-driven metabolic dysfunction. We have characterized steatosis, inflammation, Mallory–Denk body formation with hematoxylin and eosin (H&E), and fibrosis with Trichome blue staining. The presence of hepatic fibrosis with other features of NASH described above is one of the major strengths of this model since most of the currently available NASH models do not develop microvesicular steatosis or fibrosis. Together with the other important features of NASH described above, we confirm that male LEW.1WR1 rats develop NASH and insulin resistance with a standard diet. Full article
(This article belongs to the Special Issue Feature Papers in Endocrines: 2024)
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8 pages, 1165 KiB  
Communication
Protective Activities of Growth Hormone-Releasing Hormone Antagonists against Toxin-Induced Endothelial Injury
by Saikat Fakir and Nektarios Barabutis
Endocrines 2024, 5(1), 116-123; https://doi.org/10.3390/endocrines5010008 - 18 Mar 2024
Viewed by 568
Abstract
GHRH regulates the secretion of GH from the anterior pituitary gland, previously associated with cancer progression and inflammation. An emerging body of evidence suggests that GHRHAnt support endothelial barrier function, but the mechanisms mediating these events are not completely understood. In the present [...] Read more.
GHRH regulates the secretion of GH from the anterior pituitary gland, previously associated with cancer progression and inflammation. An emerging body of evidence suggests that GHRHAnt support endothelial barrier function, but the mechanisms mediating these events are not completely understood. In the present study, it is demonstrated that the GHRHAnt JV-1-36 counteracts barrier dysfunction due to LPS or LTA treatment in HUVECs, utilizing the Dextran–FITC assay. Moreover, it is shown in BPAECs that these bacterial toxins increase ROS generation, and that this effect is counteracted by JV-1-36, which reinstates the redox balance. The possible involvement of NEK2 in the beneficial activities of GHRHAnt in IFN-γ- and LPS-triggered hyperpermeability was also assessed, since that kinase is involved in inflammatory responses. NEK2 was increased in the inflamed cells, and JV-1-36 counteracted those endothelial events. Our data support the beneficial effects of GHRHAnt in toxin-induced endothelial injury. Full article
(This article belongs to the Special Issue Feature Papers in Endocrines: 2024)
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