Regulatory Networks of Pancreatic Beta-Cell Function and Insulin Secretion: Intrinsic Mechanisms and Extrinsic Modulators

A special issue of Diabetology (ISSN 2673-4540).

Deadline for manuscript submissions: 15 June 2026 | Viewed by 732

Special Issue Editors


E-Mail Website
Guest Editor
Department of Clinical and Experimental Medicine, University of Pisa, 56126 Pisa, Italy
Interests: diabetes; physiology; obesity; lipid metabolism; human islet function; non-alcoholic fatty liver disease

E-Mail Website
Guest Editor
Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy
Interests: type 2 diabetes; pancreatic islets; insulin secretion; beta cell function; pancreatic islets morphometry; type 1 diabetes; pancreatic islets transcriptomics and proteomics; intra- and peri-pancreatic adipose tissue function and morphometry

Special Issue Information

Dear Colleagues,

We invite you to contribute to this Special Issue dedicated to exploring the “Regulatory Networks of Pancreatic Beta-Cell Function and Insulin Secretion: Intrinsic Mechanisms and Extrinsic Modulators”. Pancreatic beta-cells are a central part of glucose homeostasis, and their dysfunction is a defining feature of both type 1 and type 2 diabetes. Therefore, understanding how beta-cell activity is regulated is essential for developing new therapeutic approaches.

This Special Issue aims to highlight the complex regulatory networks governing beta-cell function, encompassing both intrinsic mechanisms—such as transcriptional and epigenetic regulation, cellular metabolism, and stress responses—and extrinsic modulators, including hormonal signals, nutrient availability, interactions in the neural and immune systems, and microbiota-derived metabolites. In particular, we aim to focus on emerging concepts such as beta-cell plasticity, inter-organ communication, and the influence of circadian rhythms on insulin secretion.

We welcome the submission of original research articles, reviews, and perspectives that address these multifaceted regulatory pathways, spanning from molecular and cellular mechanisms to physiological and pathophysiological contexts. By bringing together diverse insights and cutting-edge findings, this Special Issue aims to foster a deeper understanding of beta-cell biology and support the development of innovative strategies for diabetes prevention and therapy.

We look forward to receiving your valuable contributions.

Warm regards,

Dr. Chiara Saponaro
Dr. Mara Suleiman
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 250 words) can be sent to the Editorial Office for assessment.

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. Diabetology is an international peer-reviewed open access monthly 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 1200 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

  • beta-cell function
  • insulin secretion
  • type 2 diabetes
  • hormone secretion regulation
  • glucose homeostasis
  • beta-cell plasticity
  • islet biology
  • metabolic signaling
  • inter-organ communication

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (1 paper)

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

Other

14 pages, 4286 KB  
Brief Report
The Von Hippel–Lindau Protein (pVHL) Is Downregulated in the Pancreatic Islets of Mice with Type 2 Diabetes Induced by a High-Calorie Diet
by Alma Nelly Diaz-Herreros, Alberto Granados-Galeana, Isaí Martínez-Torres, Elba Reyes-Maldonado, Erika Rosales-Cruz, Fernando Gómez-Chávez, Gabriel Betanzos-Cabrera, Amaranta Sarai Valdez-Guerrero, Juan Carlos Cancino-Diaz and Mario Eugenio Cancino-Diaz
Diabetology 2025, 6(12), 143; https://doi.org/10.3390/diabetology6120143 - 27 Nov 2025
Viewed by 275
Abstract
Background/Objectives: Knock-out mice lacking von Hippel–Lindau protein (pVHL) in pancreatic beta cells exhibit glucose intolerance and low insulin production, indicating a possible association between pVHL and diabetes mellitus (DM). It is currently unknown whether DM causes a decrease in pVHL expression. In [...] Read more.
Background/Objectives: Knock-out mice lacking von Hippel–Lindau protein (pVHL) in pancreatic beta cells exhibit glucose intolerance and low insulin production, indicating a possible association between pVHL and diabetes mellitus (DM). It is currently unknown whether DM causes a decrease in pVHL expression. In this study, we determined the level of pVHL expression in the pancreas of mice with type 2 DM (T2DM) induced by a high-calorie diet (HCD). Methods: Mice of the C57BL/6 and BALB/c strains were fed with a HCD for 10 weeks, and another group of mice of both strains were fed a standard diet (SD). The mice were monitored for body weight and glucose levels until the end of the treatment. Immunodetection for pVHL, HIF-1α, Insulin and GLUT-1 was performed. Results: A significant increase in body weight in C57BL/6 mice fed HCD at week 10 compared to mice fed a SD (p < 0.05), with similar results for the BALB/c strain. The glucose level was significantly higher in the C57BL/6 strain and the BALB/c strain fed with HCD compared to mice on a SD (p < 0.05). There was lower pVHL and insulin expression in the pancreatic islets of both strains fed HCD. In contrast, there was higher pVHL expression in the pancreatic islets of both strains of mice fed a SD. HIF-1α and GLUT-1 expression was higher in mice fed HCD than in mice fed a SD. Conclusions: HCD-induced T2DM causes low pVHL expression in the pancreatic islets of C57BL/6 and BALB/c mice, suggesting that low pVHL expression is related to the development of T2DM in mice. Full article
Show Figures

Graphical abstract

Back to TopTop