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Pancreatic Islet Cell Biology and Islet Cell Development
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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 December 2019) | Viewed by 46413

Special Issue Editor

Prof. Dr. Po Sing Leung

E-Mail Website
Guest Editor
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
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 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

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

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Published Papers (6 papers)

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Research

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16 pages, 1441 KiB  
Article
Profiling of RNAs from Human Islet-Derived Exosomes in a Model of Type 1 Diabetes
by Preethi Krishnan, Farooq Syed, Nicole Jiyun Kang, Raghavendra G. Mirmira and Carmella Evans-Molina
Int. J. Mol. Sci. 2019, 20(23), 5903; https://doi.org/10.3390/ijms20235903 - 25 Nov 2019
Cited by 47 | Viewed by 5326
Abstract
Type 1 diabetes (T1D) is characterized by the immune-mediated destruction of insulin-producing islet β cells. Biomarkers capable of identifying T1D risk and dissecting disease-related heterogeneity represent an unmet clinical need. Toward the goal of informing T1D biomarker strategies, we profiled coding and noncoding [...] Read more.
Type 1 diabetes (T1D) is characterized by the immune-mediated destruction of insulin-producing islet β cells. Biomarkers capable of identifying T1D risk and dissecting disease-related heterogeneity represent an unmet clinical need. Toward the goal of informing T1D biomarker strategies, we profiled coding and noncoding RNAs in human islet-derived exosomes and identified RNAs that were differentially expressed under proinflammatory cytokine stress conditions. Human pancreatic islets were obtained from cadaveric donors and treated with/without IL-1β and IFN-γ. Total RNA and small RNA sequencing were performed from islet-derived exosomes to identify mRNAs, long noncoding RNAs, and small noncoding RNAs. RNAs with a fold change ≥1.3 and a p-value <0.05 were considered as differentially expressed. mRNAs and miRNAs represented the most abundant long and small RNA species, respectively. Each of the RNA species showed altered expression patterns with cytokine treatment, and differentially expressed RNAs were predicted to be involved in insulin secretion, calcium signaling, necrosis, and apoptosis. Taken together, our data identify RNAs that are dysregulated under cytokine stress in human islet-derived exosomes, providing a comprehensive catalog of protein coding and noncoding RNAs that may serve as potential circulating biomarkers in T1D. Full article
(This article belongs to the Special Issue Pancreatic Islet Cell Biology and Islet Cell Development)
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26 pages, 8073 KiB  
Article
Human Fetal Bone Marrow-Derived Mesenchymal Stem Cells Promote the Proliferation and Differentiation of Pancreatic Progenitor Cells and the Engraftment Function of Islet-Like Cell Clusters
by Xing Yu Li, Shang Ying Wu and Po Sing Leung
Int. J. Mol. Sci. 2019, 20(17), 4083; https://doi.org/10.3390/ijms20174083 - 21 Aug 2019
Cited by 15 | Viewed by 4268
Abstract
Pancreatic progenitor cells (PPCs) are the primary source for all pancreatic cells, including beta-cells, and thus the proliferation and differentiation of PPCs into islet-like cell clusters (ICCs) opens an avenue to providing transplantable islets for diabetic patients. Meanwhile, mesenchymal stem cells (MSCs) can [...] Read more.
Pancreatic progenitor cells (PPCs) are the primary source for all pancreatic cells, including beta-cells, and thus the proliferation and differentiation of PPCs into islet-like cell clusters (ICCs) opens an avenue to providing transplantable islets for diabetic patients. Meanwhile, mesenchymal stem cells (MSCs) can enhance the development and function of different cell types of interest, but their role on PPCs remains unknown. We aimed to explore the mechanism-of-action whereby MSCs induce the in vitro and in vivo PPC/ICC development by means of our established co-culture system of human PPCs with human fetal bone marrow-derived MSCs. We examined the effect of MSC-conditioned medium on PPC proliferation and survival. Meanwhile, we studied the effect of MSC co-culture enhanced PPC/ICC function in vitro and in vivo co-/transplantation. Furthermore, we identified IGF1 as a critical factor responsible for the MSC effects on PPC differentiation and proliferation via IGF1-PI3K/Akt and IGF1-MEK/ERK1/2, respectively. In conclusion, our data indicate that MSCs stimulated the differentiation and proliferation of human PPCs via IGF1 signaling, and more importantly, promoted the in vivo engraftment function of ICCs. Taken together, our protocol may provide a mechanism-driven basis for the proliferation and differentiation of PPCs into clinically transplantable islets. Full article
(This article belongs to the Special Issue Pancreatic Islet Cell Biology and Islet Cell Development)
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18 pages, 6026 KiB  
Article
Fibroblast Growth Factor 21 Stimulates Pancreatic Islet Autophagy via Inhibition of AMPK-mTOR Signaling
by Sam Tsz Wai Cheng, Stephen Yu Ting Li and Po Sing Leung
Int. J. Mol. Sci. 2019, 20(10), 2517; https://doi.org/10.3390/ijms20102517 - 22 May 2019
Cited by 26 | Viewed by 5579
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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21 pages, 1153 KiB  
Review
Insulin: The Friend and the Foe in the Development of Type 2 Diabetes Mellitus
by Nadia Rachdaoui
Int. J. Mol. Sci. 2020, 21(5), 1770; https://doi.org/10.3390/ijms21051770 - 5 Mar 2020
Cited by 124 | Viewed by 15627
Abstract
Insulin, a hormone produced by pancreatic β-cells, has a primary function of maintaining glucose homeostasis. Deficiencies in β-cell insulin secretion result in the development of type 1 and type 2 diabetes, metabolic disorders characterized by high levels of blood glucose. Type 2 diabetes [...] Read more.
Insulin, a hormone produced by pancreatic β-cells, has a primary function of maintaining glucose homeostasis. Deficiencies in β-cell insulin secretion result in the development of type 1 and type 2 diabetes, metabolic disorders characterized by high levels of blood glucose. Type 2 diabetes mellitus (T2DM) is characterized by the presence of peripheral insulin resistance in tissues such as skeletal muscle, adipose tissue and liver and develops when β-cells fail to compensate for the peripheral insulin resistance. Insulin resistance triggers a rise in insulin demand and leads to β-cell compensation by increasing both β-cell mass and insulin secretion and leads to the development of hyperinsulinemia. In a vicious cycle, hyperinsulinemia exacerbates the metabolic dysregulations that lead to β-cell failure and the development of T2DM. Insulin and IGF-1 signaling pathways play critical roles in maintaining the differentiated phenotype of β-cells. The autocrine actions of secreted insulin on β-cells is still controversial; work by us and others has shown positive and negative actions by insulin on β-cells. We discuss findings that support the concept of an autocrine action of secreted insulin on β-cells. The hypothesis of whether, during the development of T2DM, secreted insulin initially acts as a friend and contributes to β-cell compensation and then, at a later stage, becomes a foe and contributes to β-cell decompensation will be discussed. Full article
(This article belongs to the Special Issue Pancreatic Islet Cell Biology and Islet Cell Development)
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14 pages, 906 KiB  
Review
Controversial Roles of Gut Microbiota-Derived Short-Chain Fatty Acids (SCFAs) on Pancreatic β-Cell Growth and Insulin Secretion
by Jun-Li Liu, Irina Segovia, Xiao-Lin Yuan and Zu-hua Gao
Int. J. Mol. Sci. 2020, 21(3), 910; https://doi.org/10.3390/ijms21030910 - 30 Jan 2020
Cited by 58 | Viewed by 7541
Abstract
In the past 15 years, gut microbiota emerged as a crucial player in health and disease. Enormous progress was made in the analysis of its composition, even in the discovery of novel species. It is time to go beyond mere microbiota-disease associations and, [...] Read more.
In the past 15 years, gut microbiota emerged as a crucial player in health and disease. Enormous progress was made in the analysis of its composition, even in the discovery of novel species. It is time to go beyond mere microbiota-disease associations and, instead, provide more causal analyses. A key mechanism of metabolic regulation by the gut microbiota is through the production of short-chain fatty acids (SCFAs). Acting as supplemental nutrients and specific ligands of two G-protein-coupled receptors (GPCRs), they target the intestines, brain, liver, and adipose tissue, and they regulate appetite, energy expenditure, adiposity, and glucose production. With accumulating but sometimes conflicting research results, key questions emerged. Do SCFAs regulate pancreatic islets directly? What is the effect of β-cell-specific receptor deletions? What are the mechanisms used by SCFAs to regulate β-cell proliferation, survival, and secretion? The receptors FFA2/3 are normally expressed on pancreatic β-cells. Deficiency in FFA2 may have caused glucose intolerance and β-cell deficiency in mice. However, this was contrasted by a double-receptor knockout. Even more controversial are the effects of SCFAs on insulin secretion; there might be no direct effect at all. Unable to draw clear conclusions, this review reveals some of the recent controversies. Full article
(This article belongs to the Special Issue Pancreatic Islet Cell Biology and Islet Cell Development)
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13 pages, 1049 KiB  
Review
Development and Characteristics of Pancreatic Epsilon Cells
by Naoaki Sakata, Gumpei Yoshimatsu and Shohta Kodama
Int. J. Mol. Sci. 2019, 20(8), 1867; https://doi.org/10.3390/ijms20081867 - 16 Apr 2019
Cited by 21 | Viewed by 7332
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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