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

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

Deadline for manuscript submissions: closed (30 November 2020).

Special Issue Editors

Prof. Piero Marchetti

Guest Editor
University of Pisa, Pisa, Italy
Interests: Clinical diabetes; Pancreas transplantation; Insulin secretion; Endocrine pancreas; Pancreatic beta cells; Beta cell transcriptomics; Beta cell proteomics
Prof. Romano Regazzi

Co-Guest Editor
Department of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, Switzerland

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. Piero Marchetti
Guest Editor
Prof. Romano Regazzi
Co-Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.dlhwdz.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 (3 papers)

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Research

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Open AccessArticle
Metformin Preserves β-Cell Compensation in Insulin Secretion and Mass Expansion in Prediabetic Nile Rats
Int. J. Mol. Sci. 2021, 22(1), 421; https://doi.org/10.3390/ijms22010421 - 03 Jan 2021
Abstract
Prediabetes is a high-risk condition for type 2 diabetes (T2D). Pancreatic β-cells adapt to impaired glucose regulation in prediabetes by increasing insulin secretion and β-cell mass expansion. In people with prediabetes, metformin has been shown to prevent prediabetes conversion to diabetes. However, emerging [...] Read more.
Prediabetes is a high-risk condition for type 2 diabetes (T2D). Pancreatic β-cells adapt to impaired glucose regulation in prediabetes by increasing insulin secretion and β-cell mass expansion. In people with prediabetes, metformin has been shown to prevent prediabetes conversion to diabetes. However, emerging evidence indicates that metformin has negative effects on β-cell function and survival. Our previous study established the Nile rat (NR) as a model for prediabetes, recapitulating characteristics of human β-cell compensation in function and mass expansion. In this study, we investigated the action of metformin on β-cells in vivo and in vitro. A 7-week metformin treatment improved glucose tolerance by reducing hepatic glucose output and enhancing insulin secretion. Although high-dose metformin inhibited β-cell glucose-stimulated insulin secretion in vitro, stimulation of β-cell insulin secretion was preserved in metformin-treated NRs via an indirect mechanism. Moreover, β-cells in NRs receiving metformin exhibited increased endoplasmic reticulum (ER) chaperones and alleviated apoptotic unfold protein response (UPR) without changes in the expression of cell identity genes. Additionally, metformin did not suppress β-cell mass compensation or proliferation. Taken together, despite the conflicting role indicated by in vitro studies, administration of metformin does not exert a negative effect on β-cell function or cell mass and, instead, early metformin treatment may help protect β-cells from exhaustion and decompensation. Full article
(This article belongs to the Special Issue Journey inside the Beta Cells in Type 2 Diabetes)
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Open AccessArticle
Ligand-Specific Factors Influencing GLP-1 Receptor Post-Endocytic Trafficking and Degradation in Pancreatic Beta Cells
Int. J. Mol. Sci. 2020, 21(21), 8404; https://doi.org/10.3390/ijms21218404 - 09 Nov 2020
Abstract
The glucagon-like peptide-1 receptor (GLP-1R) is an important regulator of blood glucose homeostasis. Ligand-specific differences in membrane trafficking of the GLP-1R influence its signalling properties and therapeutic potential in type 2 diabetes. Here, we have evaluated how different factors combine to control the [...] Read more.
The glucagon-like peptide-1 receptor (GLP-1R) is an important regulator of blood glucose homeostasis. Ligand-specific differences in membrane trafficking of the GLP-1R influence its signalling properties and therapeutic potential in type 2 diabetes. Here, we have evaluated how different factors combine to control the post-endocytic trafficking of GLP-1R to recycling versus degradative pathways. Experiments were performed in primary islet cells, INS-1 832/3 clonal beta cells and HEK293 cells, using biorthogonal labelling of GLP-1R to determine its localisation and degradation after treatment with GLP-1, exendin-4 and several further GLP-1R agonist peptides. We also characterised the effect of a rare GLP1R coding variant, T149M, and the role of endosomal peptidase endothelin-converting enzyme-1 (ECE-1), in GLP1R trafficking. Our data reveal how treatment with GLP-1 versus exendin-4 is associated with preferential GLP-1R targeting towards a recycling pathway. GLP-1, but not exendin-4, is a substrate for ECE-1, and the resultant propensity to intra-endosomal degradation, in conjunction with differences in binding affinity, contributes to alterations in GLP-1R trafficking behaviours and degradation. The T149M GLP-1R variant shows reduced signalling and internalisation responses, which is likely to be due to disruption of the cytoplasmic region that couples to intracellular effectors. These observations provide insights into how ligand- and genotype-specific factors can influence GLP-1R trafficking. Full article
(This article belongs to the Special Issue Journey inside the Beta Cells in Type 2 Diabetes)
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Review

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Open AccessReview
tRNA Biology in the Pathogenesis of Diabetes: Role of Genetic and Environmental Factors
Int. J. Mol. Sci. 2021, 22(2), 496; https://doi.org/10.3390/ijms22020496 - 06 Jan 2021
Abstract
The global rise in type 2 diabetes results from a combination of genetic predisposition with environmental assaults that negatively affect insulin action in peripheral tissues and impair pancreatic β-cell function and survival. Nongenetic heritability of metabolic traits may be an important contributor to [...] Read more.
The global rise in type 2 diabetes results from a combination of genetic predisposition with environmental assaults that negatively affect insulin action in peripheral tissues and impair pancreatic β-cell function and survival. Nongenetic heritability of metabolic traits may be an important contributor to the diabetes epidemic. Transfer RNAs (tRNAs) are noncoding RNA molecules that play a crucial role in protein synthesis. tRNAs also have noncanonical functions through which they control a variety of biological processes. Genetic and environmental effects on tRNAs have emerged as novel contributors to the pathogenesis of diabetes. Indeed, altered tRNA aminoacylation, modification, and fragmentation are associated with β-cell failure, obesity, and insulin resistance. Moreover, diet-induced tRNA fragments have been linked with intergenerational inheritance of metabolic traits. Here, we provide a comprehensive review of how perturbations in tRNA biology play a role in the pathogenesis of monogenic and type 2 diabetes. Full article
(This article belongs to the Special Issue Journey inside the Beta Cells in Type 2 Diabetes)
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