ijms-logo

Journal Browser

Journal Browser

Molecular Endocrinology and Molecular Markers in Animals

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (30 April 2021) | Viewed by 3157

Special Issue Editors


E-Mail Website
Guest Editor
1. MIGAL—Galilee Research Institute, Kiryat Shmona 1101602, Israel
2. Faculty of Sciences, Tel-Hai College, Upper Galilee, Kiryat Shmona 1220800, Israel
Interests: gene expression mechanisms in hormonal control of fish growth and reproduction; animals and fish in the ecological system and environmental effects on habitat selection; fish and amphibian nutrition; molecular markers in fish; aquacultural biotechnology
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
1. Principal Investigator at MIGAL - Galilee Research Institute, Kiryat Shmona, Israel
2. Lecturer at Tel Hai Academic College, Qiryat Shemona, Israel
3. Visiting Researcher at the Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark
Interests: diabetes; noncoding RNAs; microRNAs; transcriptomics; molecular mechanisms of metabolic diseases and cancer; molecular links between chronic diseases; biomarkers
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue will focus on molecular endocrinology and molecular markers involved in animal research; the gene expression regulatory mechanisms involved in the hormonal control of animal growth and reproduction; the genes involved in controlling gonadal development and changes during the reproduction cycle; interaction between gene expression in the brain, pituitary, and gonad hormone axis (BPG) in animals during growth and reproduction; molecular markers in animals for sex differentiation and sex determination; whole-genome and transcriptome studies in BPG and their application to agriculture.

 

Prof. Dr. Gad Degani

Dr. Ari Meerson
Guest Editor

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • aquaculture
  • gene expiration
  • brain pituitary and gonad axis (BPG)
  • fish
  • amphibian
  • reptilian
  • birds
  • mammals
  • sex determination
  • sex differentiation
  • hormones

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

14 pages, 13329 KiB  
Article
Calcium-Sensing Receptor in Adipose Tissue: Possible Association with Obesity-Related Elevated Autophagy
by Pamela Mattar, Sofía Sanhueza, Gabriela Yuri, Lautaro Briones, Claudio Perez-Leighton, Assaf Rudich, Sergio Lavandero and Mariana Cifuentes
Int. J. Mol. Sci. 2020, 21(20), 7617; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21207617 - 15 Oct 2020
Cited by 10 | Viewed by 2686
Abstract
Autophagy is upregulated in adipose tissue (AT) from people with obesity. We showed that activation of the calcium-sensing receptor (CaSR) elevates proinflammatory cytokines through autophagy in preadipocytes. Our aim is to understand the role of CaSR on autophagy in AT from humans with [...] Read more.
Autophagy is upregulated in adipose tissue (AT) from people with obesity. We showed that activation of the calcium-sensing receptor (CaSR) elevates proinflammatory cytokines through autophagy in preadipocytes. Our aim is to understand the role of CaSR on autophagy in AT from humans with obesity. We determined mRNA and protein levels of CaSR and markers of autophagy by qPCR and western blot in human visceral AT explants or isolated primary preadipocytes (60 donors: 72% female, 23–56% body fat). We also investigated their association with donors’ anthropometric variables. Donors’ % body fat and CaSR mRNA expression in AT were correlated (r = 0.44, p < 0.01). CaSR expression was associated with mRNA levels of the autophagy markers atg5 (r = 0.37, p < 0.01), atg7 (r = 0.29, p < 0.05) and lc3b (r = 0.40, p < 0.01). CaSR activation increased becn and atg7 mRNA expression in AT. CaSR activation also upregulated LC3II by ~50%, an effect abolished by the CaSR inhibitor. Spermine (CaSR agonist) regulates LC3II through the ERK1/2 pathway. Structural equation model analysis suggests a link between donors’ AT CaSR expression, AT autophagy and expression of Tumor Necrosis Factor alpha TNF-α. CaSR expression in visceral AT is directly associated with % body fat, and CaSR activation may contribute to obesity-related disruption in AT autophagy. Full article
(This article belongs to the Special Issue Molecular Endocrinology and Molecular Markers in Animals)
Show Figures

Figure 1

Back to TopTop