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Special Issue "Pancreatic Islet Cell Biology and Islet Cell Development"

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

Deadline for manuscript submissions: closed (31 January 2019)

Special Issue Editor

Guest Editor
Prof. Dr. Po Sing Leung

Lo Kwee-Seong Integrated Biomedical Sciences Building, School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong
Website | E-Mail
Interests: pancreatic islet cell biology; pancreatic stem cell research; islet transplantation; diabetes

Special Issue Information

Dear Colleagues,

Normal pancreatic islet cell function and cell survival are two key determinants in the maintenace of islet cell biology and health, and thus its abnormalities lead to disease, as seen in type 1 and type 2 diabetes mellitus. A thorough investigation into novel factors that improve islet b-cell secretion and b-cell mass expansion is thus indispensable for islet health before diabetes can be treated or even cured by pharmacological or non-pharmacological interventions.

In view of this fact, targeting at islet studies is central to the prevention and therapeutic option of human diabetes. While a fuller understanding of islet physiology provides extensive, as yet unexplored information, a detailed exploitation of islet development will provide a mechanism-based approach to offering functionally driven b-cells for clinical islet transplantation as well as facilitating formulation of novel agents/drugs for diabetes.

This Special Issue entilted “Pancreatic Islet Cell Biology and Islet Cell Development” is aiming at providing a research platform for the collection of high quaity, up-to-date original and review articles that cover various aspects of cellular and molecular biology of islet cell studies in health and disease, particularly those factors that enhance b-cell function and development with translational potential.

Prof. Dr. Po Sing Leung
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 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. The Article Processing Charge (APC) for publication in this open access journal is 1800 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

  • Insulin secretion
  • islet function
  • islet survival
  • pancreatic stem cells
  • β-cell proliferation
  • β-cell differentiation
  • FGF21
  • GPR120
  • obesity
  • diabetes
  • pancreas

Published Papers (2 papers)

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Research

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Open AccessArticle
Fibroblast Growth Factor 21 Stimulates Pancreatic Islet Autophagy via Inhibition of AMPK-mTOR Signaling
Int. J. Mol. Sci. 2019, 20(10), 2517; https://doi.org/10.3390/ijms20102517 (registering DOI)
Received: 24 April 2019 / Revised: 17 May 2019 / Accepted: 21 May 2019 / Published: 22 May 2019
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Abstract
Background: Islet autophagy plays a role in glucose/lipid metabolism in type 2 diabetes mellitus. Meanwhile, fibroblast growth factor 21 (FGF21) has been found to regulate insulin sensitivity and glucose homeostasis. Whether FGF21 induces islet autophagy, remains to be elucidated. This study aimed to [...] Read more.
Background: Islet autophagy plays a role in glucose/lipid metabolism in type 2 diabetes mellitus. Meanwhile, fibroblast growth factor 21 (FGF21) has been found to regulate insulin sensitivity and glucose homeostasis. Whether FGF21 induces islet autophagy, remains to be elucidated. This study aimed to explore the physiological roles and signaling pathways involved in FGF21-stimulated islet autophagy under glucolipotoxic conditions. Methods: C57/BL6J mice were fed a standard diet or high-fat diet (HFD) for 12 weeks, and islets were isolated from normal and FGF21 knockout (KO) mice. Isolated islets and INS-1E cells were exposed to normal and high-concentration glucose and palmitic acid with/without FGF21 or AMPK inhibitor compound C. Real-time PCR, Western blot and immunohistochemistry/transmission electron microscopy were performed for the expression of targeted genes/proteins. Results: HFD-treated mice showed increases in fasting plasma glucose, body weight and impaired glucose tolerance; islet protein expression of FGF21 was induced after HFD treatment. Protein expression levels of FGF21 and LC3-II (autophagy marker) were induced in mouse islets treated with high concentrations of palmitic acid and glucose, while phosphorylation of AMPK was reduced, compared with controls. In addition, induction of LC3-II protein expression was reduced in islets isolated from FGF21 KO mice. Furthermore, exogenous administration of FGF21 diminished phosphorylation of AMPK and stimulated protein expression of LC3-II. Consistently, compound C significantly induced increased expression of LC3-II protein. Conclusions: Our data indicate that glucolipotoxicity-induced FGF21 activation mediates islet autophagy via AMPK inhibition, and further consolidate the evidence for the FGF21/analog being a pharmacotherapeutic target for obesity and its related T2DM. Full article
(This article belongs to the Special Issue Pancreatic Islet Cell Biology and Islet Cell Development)
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Review

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Open AccessReview
Development and Characteristics of Pancreatic Epsilon Cells
Int. J. Mol. Sci. 2019, 20(8), 1867; https://doi.org/10.3390/ijms20081867
Received: 4 April 2019 / Revised: 11 April 2019 / Accepted: 12 April 2019 / Published: 16 April 2019
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Abstract
Pancreatic endocrine cells expressing the ghrelin gene and producing the ghrelin hormone were first identified in 2002. These cells, named ε cells, were recognized as the fifth type of endocrine cells. Differentiation of ε cells is induced by various transcription factors, including Nk2 [...] Read more.
Pancreatic endocrine cells expressing the ghrelin gene and producing the ghrelin hormone were first identified in 2002. These cells, named ε cells, were recognized as the fifth type of endocrine cells. Differentiation of ε cells is induced by various transcription factors, including Nk2 homeobox 2, paired box proteins Pax-4 and Pax6, and the aristaless-related homeobox. Ghrelin is generally considered to be a “hunger hormone” that stimulates the appetite and is produced mainly by the stomach. Although the population of ε cells is small in adults, they play important roles in regulating other endocrine cells, especially β cells, by releasing ghrelin. However, the roles of ghrelin in β cells are complex. Ghrelin contributes to increased blood glucose levels by suppressing insulin release from β cells and is also involved in the growth and proliferation of β cells and the prevention of β cell apoptosis. Despite increasing evidence and clarification of the mechanisms of ε cells over the last 20 years, many questions remain to be answered. In this review, we present the current evidence for the participation of ε cells in differentiation and clarify their characteristics by focusing on the roles of ghrelin. Full article
(This article belongs to the Special Issue Pancreatic Islet Cell Biology and Islet Cell Development)
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Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
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