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Special Issue "Journey inside the Beta Cells in Type 2 Diabetes-2nd Edition"

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: 31 October 2021.

Special Issue Editors

Prof. Dr. Piero Marchetti
E-Mail Website
Guest Editor
Department of Clinical and Experimental Medicine, University of Pisa, 56126 Pisa, Italy
Interests: Clinical diabetes; Pancreas transplantation; Insulin secretion; Endocrine pancreas; Pancreatic beta cells; Beta cell transcriptomics; Beta cell proteomics
Special Issues and Collections in MDPI journals
Prof. Dr. Romano Regazzi
E-Mail Website
Guest Editor
Department of Fundamental Neurosciences, Universitat Lausanne Schweiz, Lausanne, Switzerland
Interests: β-cell dysfunction; noncoding RNAs; islet

Special Issue Information

Dear Colleagues,

Pancreatic beta cell failure is key to the onset and progression of type 2 diabetes (T2D; the most common form of this heterogeneous disease), due to the interplay of genetic and environmental determinants. Loss of identity, secretory dysfunction, increased demise and meager regeneration are the main shortcomings of the beta cells in T2D, leading to insufficient insulin release and increased blood glucose levels. Over the past few years, our understanding of the mechanisms underlying beta cell defects in T2D has greatly expanded. Histological, functional, survival, genetic, epigenetic and “omics” data have made it possible to elaborate on the cellular and molecular processes responsible for beta cell sickness. Yet, the scenario remains unclear, due to the complexity of the beta cells and the variability of some of their phenotypic features. This Special Issue has the ambition to reconcile some of the diverse views currently available, with its main focus on the human setting. Molecular “sightseeings” will be interpreted in respect of the commitments of key intracellular compartments, in order to give a more integrated overview of the beta cell interior. Hints on potential prevention and targeted treatment strategies will also be provided, as an attempt to move our knowledge of beta cell fatigue in T2D toward translational applications.

Prof. Dr. Piero Marchetti
Prof. Dr. Romano Regazzi
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 papers will be 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

  • type 2 diabetes
  • insulin secretion
  • pancreatic beta cells
  • beta cell “omics”
  • Golgi apparatus
  • endoplasmic reticulum
  • mitochondria
  • exocytosis

Published Papers (1 paper)

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Review

Review
Beta-Cell Dysfunction Induced by Tacrolimus: A Way to Explain Type 2 Diabetes?
Int. J. Mol. Sci. 2021, 22(19), 10311; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms221910311 - 24 Sep 2021
Viewed by 336
Abstract
The combination of insulin resistance and β-cells dysfunction leads to the onset of type-2 diabetes mellitus (T2DM). This process can last for decades, as β-cells are able to compensate the demand for insulin and maintain normoglycemia. Understanding the adaptive capacity of β-cells during [...] Read more.
The combination of insulin resistance and β-cells dysfunction leads to the onset of type-2 diabetes mellitus (T2DM). This process can last for decades, as β-cells are able to compensate the demand for insulin and maintain normoglycemia. Understanding the adaptive capacity of β-cells during this process and the causes of its failure is essential to the limit onset of diabetes. Post-transplant diabetes mellitus (PTDM) is a common and serious disease that affects 30% of renal transplant recipients. With the exception of immunosuppressive therapy, the risk factors for T2D are the same as for PTDM: obesity, dyslipidaemia, insulin resistance and metabolic syndrome. Tacrolimus (TAC) is the immunosuppressant of choice after renal transplantation but it has the highest rates of PTDM. Our group has shown that insulin resistance and glucolipotoxicity, without favouring the appearance of apoptosis, modify key nuclear factors for the maintenance of identity and functionality of β-cells. In this context, TAC accelerates or enhances these changes. Our hypothesis is that the pathways that are affected in the progression from pre-diabetes to diabetes in the general population are the same pathways that are affected by TAC. So, TAC can be considered a tool to study the pathogenesis of T2DM. Here, we review the common pathways of β-cells dysfunction on T2DM and TAC-induced diabetes. Full article
(This article belongs to the Special Issue Journey inside the Beta Cells in Type 2 Diabetes-2nd Edition)
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