Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
7.8
5.6
Journals
IJMS
Special Issues
Journey inside the Beta Cells in Type 2 Diabetes-2nd Edition
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

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: closed (31 July 2022) | Viewed by 24434

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, Collections and Topics in MDPI journals
Prof. Dr. Romano Regazzi

E-Mail Website
Guest Editor
Department of Fundamental Neurosciences, University of Lausanne, 1005 Lausanne, Switzerland
Interests: β-cell dysfunction; noncoding RNAs; islet
Special Issues, Collections and Topics in MDPI journals

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 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

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

Published Papers (7 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Review

11 pages, 496 KiB  
Review
The Role of Beta Cell Recovery in Type 2 Diabetes Remission
by Mara Suleiman, Lorella Marselli, Miriam Cnop, Decio L. Eizirik, Carmela De Luca, Francesca R. Femia, Marta Tesi, Silvia Del Guerra and Piero Marchetti
Int. J. Mol. Sci. 2022, 23(13), 7435; https://doi.org/10.3390/ijms23137435 - 4 Jul 2022
Cited by 16 | Viewed by 5109
Abstract
Type 2 diabetes (T2D) has been considered a relentlessly worsening disease, due to the progressive deterioration of the pancreatic beta cell functional mass. Recent evidence indicates, however, that remission of T2D may occur in variable proportions of patients after specific treatments that are [...] Read more.
Type 2 diabetes (T2D) has been considered a relentlessly worsening disease, due to the progressive deterioration of the pancreatic beta cell functional mass. Recent evidence indicates, however, that remission of T2D may occur in variable proportions of patients after specific treatments that are associated with recovery of beta cell function. Here we review the available information on the recovery of beta cells in (a) non-diabetic individuals previously exposed to metabolic stress; (b) T2D patients following low-calorie diets, pharmacological therapies or bariatric surgery; (c) human islets isolated from non-diabetic organ donors that recover from “lipo-glucotoxic” conditions; and (d) human islets isolated from T2D organ donors and exposed to specific treatments. The improvement of insulin secretion reported by these studies and the associated molecular traits unveil the possibility to promote T2D remission by directly targeting pancreatic beta cells. Full article
(This article belongs to the Special Issue Journey inside the Beta Cells in Type 2 Diabetes-2nd Edition)
►▼ Show Figures

Figure 1

20 pages, 8501 KiB  
Review
Mechanisms Underlying the Expansion and Functional Maturation of β-Cells in Newborns: Impact of the Nutritional Environment
by Cécile Jacovetti and Romano Regazzi
Int. J. Mol. Sci. 2022, 23(4), 2096; https://doi.org/10.3390/ijms23042096 - 14 Feb 2022
Cited by 7 | Viewed by 3422
Abstract
The functional maturation of insulin-secreting β-cells is initiated before birth and is completed in early postnatal life. This process has a critical impact on the acquisition of an adequate functional β-cell mass and on the capacity to meet and adapt to insulin needs [...] Read more.
The functional maturation of insulin-secreting β-cells is initiated before birth and is completed in early postnatal life. This process has a critical impact on the acquisition of an adequate functional β-cell mass and on the capacity to meet and adapt to insulin needs later in life. Many cellular pathways playing a role in postnatal β-cell development have already been identified. However, single-cell transcriptomic and proteomic analyses continue to reveal new players contributing to the acquisition of β-cell identity. In this review, we provide an updated picture of the mechanisms governing postnatal β-cell mass expansion and the transition of insulin-secreting cells from an immature to a mature state. We then highlight the contribution of the environment to β-cell maturation and discuss the adverse impact of an in utero and neonatal environment characterized by calorie and fat overload or by protein deficiency and undernutrition. Inappropriate nutrition early in life constitutes a risk factor for developing diabetes in adulthood and can affect the β-cells of the offspring over two generations. A better understanding of these events occurring in the neonatal period will help developing better strategies to produce functional β-cells and to design novel therapeutic approaches for the prevention and treatment of diabetes. Full article
(This article belongs to the Special Issue Journey inside the Beta Cells in Type 2 Diabetes-2nd Edition)
►▼ Show Figures

Figure 1

23 pages, 834 KiB  
Review
Apoptosis in Type 2 Diabetes: Can It Be Prevented? Hippo Pathway Prospects
by Agnieszka Kilanowska and Agnieszka Ziółkowska
Int. J. Mol. Sci. 2022, 23(2), 636; https://doi.org/10.3390/ijms23020636 - 7 Jan 2022
Cited by 8 | Viewed by 3620
Abstract
Diabetes mellitus is a heterogeneous disease of complex etiology and pathogenesis. Hyperglycemia leads to many serious complications, but also directly initiates the process of β cell apoptosis. A potential strategy for the preservation of pancreatic β cells in diabetes may be to inhibit [...] Read more.
Diabetes mellitus is a heterogeneous disease of complex etiology and pathogenesis. Hyperglycemia leads to many serious complications, but also directly initiates the process of β cell apoptosis. A potential strategy for the preservation of pancreatic β cells in diabetes may be to inhibit the implementation of pro-apoptotic pathways or to enhance the action of pancreatic protective factors. The Hippo signaling pathway is proposed and selected as a target to manipulate the activity of its core proteins in therapy-basic research. MST1 and LATS2, as major upstream signaling kinases of the Hippo pathway, are considered as target candidates for pharmacologically induced tissue regeneration and inhibition of apoptosis. Manipulating the activity of components of the Hippo pathway offers a wide range of possibilities, and thus is a potential tool in the treatment of diabetes and the regeneration of β cells. Therefore, it is important to fully understand the processes involved in apoptosis in diabetic states and completely characterize the role of this pathway in diabetes. Therapy consisting of slowing down or stopping the mechanisms of apoptosis may be an important direction of diabetes treatment in the future. Full article
(This article belongs to the Special Issue Journey inside the Beta Cells in Type 2 Diabetes-2nd Edition)
►▼ Show Figures

Figure 1

17 pages, 1775 KiB  
Review
Lipid-Induced Adaptations of the Pancreatic Beta-Cell to Glucotoxic Conditions Sustain Insulin Secretion
by Lucie Oberhauser and Pierre Maechler
Int. J. Mol. Sci. 2022, 23(1), 324; https://doi.org/10.3390/ijms23010324 - 28 Dec 2021
Cited by 9 | Viewed by 3799
Abstract
Over the last decades, lipotoxicity and glucotoxicity emerged as established mechanisms participating in the pathophysiology of obesity-related type 2 diabetes in general, and in the loss of β-cell function in particular. However, these terms hold various potential biological processes, and it is not [...] Read more.
Over the last decades, lipotoxicity and glucotoxicity emerged as established mechanisms participating in the pathophysiology of obesity-related type 2 diabetes in general, and in the loss of β-cell function in particular. However, these terms hold various potential biological processes, and it is not clear what precisely they refer to and to what extent they might be clinically relevant. In this review, we discuss the basis and the last advances of research regarding the role of free fatty acids, their metabolic intracellular pathways, and receptor-mediated signaling related to glucose-stimulated insulin secretion, as well as lipid-induced β-cell dysfunction. We also describe the role of chronically elevated glucose, namely, glucotoxicity, which promotes failure and dedifferentiation of the β cell. Glucolipotoxicity combines deleterious effects of exposures to both high glucose and free fatty acids, supposedly provoking synergistic defects on the β cell. Nevertheless, recent studies have highlighted the glycerolipid/free fatty acid cycle as a protective pathway mediating active storage and recruitment of lipids. Finally, we discuss the putative correspondence of the loss of functional β cells in type 2 diabetes with a natural, although accelerated, aging process. Full article
(This article belongs to the Special Issue Journey inside the Beta Cells in Type 2 Diabetes-2nd Edition)
►▼ Show Figures

Figure 1

17 pages, 4386 KiB  
Review
β-Cell Pathophysiology: A Review of Advanced Optical Microscopy Applications
by Gianmarco Ferri, Luca Pesce, Marta Tesi, Piero Marchetti and Francesco Cardarelli
Int. J. Mol. Sci. 2021, 22(23), 12820; https://doi.org/10.3390/ijms222312820 - 26 Nov 2021
Cited by 4 | Viewed by 1846
Abstract
β-cells convert glucose (input) resulting in the controlled release of insulin (output), which in turn has the role to maintain glucose homeostasis. β-cell function is regulated by a complex interplay between the metabolic processing of the input, its transformation into second-messenger signals, and [...] Read more.
β-cells convert glucose (input) resulting in the controlled release of insulin (output), which in turn has the role to maintain glucose homeostasis. β-cell function is regulated by a complex interplay between the metabolic processing of the input, its transformation into second-messenger signals, and final mobilization of insulin-containing granules towards secretion of the output. Failure at any level in this process marks β-cell dysfunction in diabetes, thus making β-cells obvious potential targets for therapeutic purposes. Addressing quantitatively β-cell (dys)function at the molecular level in living samples requires probing simultaneously the spatial and temporal dimensions at the proper resolution. To this aim, an increasing amount of research efforts are exploiting the potentiality of biophysical techniques. In particular, using excitation light in the visible/infrared range, a number of optical-microscopy-based approaches have been tailored to the study of β-cell-(dys)function at the molecular level, either in label-free mode (i.e., exploiting intrinsic autofluorescence of cells) or by the use of organic/genetically-encoded fluorescent probes. Here, relevant examples from the literature are reviewed and discussed. Based on this, new potential lines of development in the field are drawn. Full article
(This article belongs to the Special Issue Journey inside the Beta Cells in Type 2 Diabetes-2nd Edition)
►▼ Show Figures

Figure 1

11 pages, 4888 KiB  
Review
Arginase 2 and Polyamines in Human Pancreatic Beta Cells: Possible Role in the Pathogenesis of Type 2 Diabetes
by Lorella Marselli, Emanuele Bosi, Carmela De Luca, Silvia Del Guerra, Marta Tesi, Mara Suleiman and Piero Marchetti
Int. J. Mol. Sci. 2021, 22(22), 12099; https://doi.org/10.3390/ijms222212099 - 9 Nov 2021
Cited by 6 | Viewed by 2253
Abstract
Arginase 2 (ARG2) is a manganese metalloenzyme involved in several tissue specific processes, from physiology to pathophysiology. It is variably expressed in extra-hepatic tissues and is located in the mitochondria. In human pancreatic beta cells, ARG2 is downregulated in type 2 diabetes. The [...] Read more.
Arginase 2 (ARG2) is a manganese metalloenzyme involved in several tissue specific processes, from physiology to pathophysiology. It is variably expressed in extra-hepatic tissues and is located in the mitochondria. In human pancreatic beta cells, ARG2 is downregulated in type 2 diabetes. The enzyme regulates the synthesis of polyamines, that are involved in pancreas development and regulation of beta cell function. Here, we discuss several features of ARG2 and polyamines, which can be relevant to the pathophysiology of type 2 diabetes. Full article
(This article belongs to the Special Issue Journey inside the Beta Cells in Type 2 Diabetes-2nd Edition)
►▼ Show Figures

Figure 1

14 pages, 1487 KiB  
Review
Beta-Cell Dysfunction Induced by Tacrolimus: A Way to Explain Type 2 Diabetes?
by Ana Elena Rodriguez-Rodriguez, Esteban Porrini and Armando Torres
Int. J. Mol. Sci. 2021, 22(19), 10311; https://doi.org/10.3390/ijms221910311 - 24 Sep 2021
Cited by 18 | Viewed by 3373
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)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-7
Back to TopTop