Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
9.4
4.8
Journals
Biomolecules
Special Issues
Pancreatic Islets of Langerhans: Not Only Beta-Cells
share announcement

Pancreatic Islets of Langerhans: Not Only Beta-Cells

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (30 June 2021) | Viewed by 31158

Special Issue Editors

Prof. Dr. Roberta Malaguarnera

E-Mail Website
Guest Editor
School of Human and Social Sciences, "Kore" University of Enna, 94100 Enna, Italy
Interests: insulin receptor and signaling; IGFs system; endocrine-related cancers; stem cells; sex hormones signaling; diabetes; mTOR; p53; nutrition and physical activity
Prof. Dr. Salvatore Piro

E-Mail Website
Guest Editor
Department of Clinical and Experimental Medicine, University of Catania, 95122 Catania, Italy
Interests: diabetes; glucagon; incretin; NAFLD; NASH; insulin resistance; pancreatic islets; pancreatic glucotoxicity and lipotoxicity; hypercholesterolemia; GLP-1 analogs; DDP4 inhibitors
Dr. Antonino Di Pino

E-Mail Website
Guest Editor
Department of Clinical and Experimental Medicine, University of Catania, 95122 Catania, Italy
Interests: atherosclerosis; prediabetes; metabolic syndrome; hypercholesterolemia; hypertension; glucagon; lipids; advanced glycation end-products; liver diseases

Special Issue Information

Dear Colleagues,

Pancreatic islets constitute the endocrine portion of the pancreas containing different types of cells secreting several hormones in addition to insulin, such as glucagon, GLP-1, somatostatin, and pancreatic polypeptide. Since 1921, the year in which insulin was discovered, the history of diabetes has focused only on this hormone as the main regulator of glucose homeostasis. It has recently become understood that, in fact, all of the hormones produced by pancreatic islets interact each other through paracrine and autocrine loops and communicate in an endocrine manner with other organs to regulate glucose, lipid, and protein metabolism. In light of this new understanding of endocrine and metabolic pathophysiology, the importance of glucagon—as a hormone with pleiotropic action that goes far beyond the regulation of glucose metabolism—has been reconsidered. In particular, understanding of the role of glucagon in the interactions with other organs (such as liver, adipose tissue, skeletal muscle, heart, gut, brain, pancreas, and kidney),  the canonical incretin axis (i.e., GIP, GLP-1, and GLP1-R), and pro-inflammatory cytokines (i.e., IL-6) as well as the knowledge of glucagon’s involvement in thermogenesis, food intake, energy expenditure, satiety, and bile acid metabolism have opened new perspectives for the management and treatment of diabetic/obesity diseases and their complications (i.e., hypercholesterolemia, hypertension, and cardiovascular diseases). Furthermore, the finding that the secretion of most of pancreatic hormones, including glucagon, is regulated by a large number of G-protein-coupled receptors (GPCRs) has prompted reevaluation of the role of glucagon in different classes of drugs used to treat type-2 diabetes and obesity.

We welcome original as well as review articles on a broad range of topics related to glucagon and/or other pancreatic hormones (apart from insulin) and to the molecular and clinical implications of the mutual crosstalk between the endocrine pancreatic islets axis and peripheral tissues.

Prof. Dr. Roberta Malaguarnera
Prof. Dr. Salvatore Piro
Dr. Antonino Di Pino
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. Biomolecules 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 2700 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

  • pancreatic islets
  • glucagon
  • insulin
  • incretin
  • diabetes
  • obesity
  • peripheral tissues

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.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

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

Published Papers (8 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:

Editorial

Jump to: Research, Review

3 pages, 173 KiB  
Editorial
Editorial on the Special Issue: “Pancreatic Islets of Langerhans: Not Only Beta-Cells”
by Roberta Malaguarnera and Salvatore Piro
Biomolecules 2021, 11(11), 1646; https://doi.org/10.3390/biom11111646 - 7 Nov 2021
Viewed by 1483
Abstract
This year marks the centenary of the discovery of insulin [...] Full article
(This article belongs to the Special Issue Pancreatic Islets of Langerhans: Not Only Beta-Cells)

Research

Jump to: Editorial, Review

12 pages, 10422 KiB  
Article
A Systematic Comparison of Protocols for Recovery of High-Quality RNA from Human Islets Extracted by Laser Capture Microdissection
by Chiara M. A. Cefalo, Teresa Mezza, Andrea Giaccari and Rohit N. Kulkarni
Biomolecules 2021, 11(5), 625; https://doi.org/10.3390/biom11050625 - 22 Apr 2021
Cited by 5 | Viewed by 2956
Abstract
The isolation of high-quality RNA from endocrine pancreas sections represents a considerable challenge largely due to the high ribonuclease levels. Laser capture microdissection (LCM) of mammalian islets, in association with RNA extraction protocols, has emerged as a feasible approach to characterizing their genetic [...] Read more.
The isolation of high-quality RNA from endocrine pancreas sections represents a considerable challenge largely due to the high ribonuclease levels. Laser capture microdissection (LCM) of mammalian islets, in association with RNA extraction protocols, has emerged as a feasible approach to characterizing their genetic and proteomic profiles. However, a validated protocol to obtain high-quality RNA from LCM-derived human pancreas specimens that is appropriate for next-generation sequencing analysis is still lacking. In this study, we applied four methods (Picopure extraction kit, Qiazol protocol, Qiazol + Clean-up kit, and RNeasy Microkit + Carrier) to extract RNA from human islets obtained from both non-diabetic individuals and patients with type 2 diabetes who had undergone partial pancreatectomy, as well as handpicked islets from both non-diabetic and diabetic organ donors. The yield and purity of total RNA were determined by 260/280 absorbance using Nanodrop 100 and the RNA integrity number with a bioanalyzer. The results indicated that among the four methods, the RNeasy MicroKit + Carrier (Qiagen) provides the highest yield and purity. Full article
(This article belongs to the Special Issue Pancreatic Islets of Langerhans: Not Only Beta-Cells)
►▼ Show Figures

Figure 1

10 pages, 1610 KiB  
Article
Pro-Inflammatory Cytokines Induce Insulin and Glucagon Double Positive Human Islet Cells That Are Resistant to Apoptosis
by Marta Tesi, Marco Bugliani, Gianmarco Ferri, Mara Suleiman, Carmela De Luca, Emanuele Bosi, Matilde Masini, Vincenzo De Tata, Conny Gysemans, Francesco Cardarelli, Miriam Cnop, Decio L. Eizirik, Piero Marchetti and Lorella Marselli
Biomolecules 2021, 11(2), 320; https://doi.org/10.3390/biom11020320 - 19 Feb 2021
Cited by 10 | Viewed by 3878
Abstract
The presence of islet cells double positive for insulin and glucagon (Ins+/Glu+) has been described in the pancreas from both type 2 (T2D) and type 1 (T1D) diabetic subjects. We studied the role of pro-inflammatory cytokines on the occurrence, [...] Read more.
The presence of islet cells double positive for insulin and glucagon (Ins+/Glu+) has been described in the pancreas from both type 2 (T2D) and type 1 (T1D) diabetic subjects. We studied the role of pro-inflammatory cytokines on the occurrence, trajectory, and characteristics of Ins+/Glu+ cells in human pancreatic islets. Pancreas samples, isolated islets, and dispersed islet cells from 3 T1D and 11 non-diabetic (ND) multi-organ donors were studied by immunofluorescence, confocal microscopy, and/or electron microscopy. ND islet cells were exposed to interleukin-1β and interferon-γ for up to 120 h. In T1D islets, we confirmed an increased prevalence of Ins+/Glu+ cells. Cytokine-exposed islets showed a progressive increase of Ins+/Glu+ cells that represented around 50% of endocrine cells after 120h. Concomitantly, cells expressing insulin granules only decreased significantly over time, whereas those containing only glucagon granules remained stable. Interestingly, Ins+/Glu+ cells were less prone to cytokine-induced apoptosis than cells containing only insulin. Cytokine-exposed islets showed down-regulation of β-cell identity genes. In conclusion, pro-inflammatory cytokines induce Ins+/Glu+ cells in human islets, possibly due to a switch from a β- to a β-/α-cell phenotype. These Ins+/Glu+ cells appear to be resistant to cytokine-induced apoptosis. Full article
(This article belongs to the Special Issue Pancreatic Islets of Langerhans: Not Only Beta-Cells)
►▼ Show Figures

Figure 1

12 pages, 9456 KiB  
Article
Glucagon Prevents Cytotoxicity Induced by Methylglyoxal in a Rat Neuronal Cell Line Model
by Mohammad Sarif Mohiuddin, Tatsuhito Himeno, Yuichiro Yamada, Yoshiaki Morishita, Masaki Kondo, Shin Tsunekawa, Yoshiro Kato, Jiro Nakamura and Hideki Kamiya
Biomolecules 2021, 11(2), 287; https://doi.org/10.3390/biom11020287 - 15 Feb 2021
Cited by 15 | Viewed by 3496
Abstract
Although diabetic polyneuropathy (DPN) is a frequent diabetic complication, no effective therapeutic approach has been established. Glucagon is a crucial hormone for glucose homeostasis but has pleiotropic effects, including neuroprotective effects in the central nervous system. However, the importance of glucagon in the [...] Read more.
Although diabetic polyneuropathy (DPN) is a frequent diabetic complication, no effective therapeutic approach has been established. Glucagon is a crucial hormone for glucose homeostasis but has pleiotropic effects, including neuroprotective effects in the central nervous system. However, the importance of glucagon in the peripheral nervous system (PNS) has not been clarified. Here, we hypothesized that glucagon might have a neuroprotective function in the PNS. The immortalized rat dorsal root ganglion (DRG) neuronal cell line 50B11 was treated with methylglyoxal (MG) to mimic an in vitro DPN model. The cells were cultured with or without glucagon or MG. Neurotoxicity, survival, apoptosis, neurite projection, cyclic adenosine monophosphate (cAMP), and protein kinase A (PKA) were examined. Glucagon had no cytotoxicity and rescued the cells from neurotoxicity. Cell survival was increased by glucagon. The ratio of apoptotic cells, which was increased by MG, was reduced by glucagon. Neurite outgrowth was accelerated in glucagon-treated cells. Cyclic AMP and PKA accumulated in the cells after glucagon stimulation. In conclusion, glucagon protected the DRG neuronal cells from MG-induced cellular stress. The cAMP/PKA pathway may have significant roles in those protective effects of glucagon. Glucagon may be a potential target for the treatment of DPN. Full article
(This article belongs to the Special Issue Pancreatic Islets of Langerhans: Not Only Beta-Cells)
►▼ Show Figures

Figure 1

15 pages, 2096 KiB  
Article
Direct Effects of D-Chiro-Inositol on Insulin Signaling and Glucagon Secretion of Pancreatic Alpha Cells
by Agnese Filippello, Alessandra Scamporrino, Stefania Di Mauro, Roberta Malaguarnera, Antonino Di Pino, Roberto Scicali, Francesco Purrello and Salvatore Piro
Biomolecules 2020, 10(10), 1404; https://doi.org/10.3390/biom10101404 - 4 Oct 2020
Cited by 11 | Viewed by 3790
Abstract
The insulin resistance state of pancreatic α-cells seems to be related to glucagon hypersecretion in type 2 diabetes. Treatment that can improve the insulin sensitivity of α-cells could control glucagon levels in patients with diabetes mellitus. The aim of this study was to [...] Read more.
The insulin resistance state of pancreatic α-cells seems to be related to glucagon hypersecretion in type 2 diabetes. Treatment that can improve the insulin sensitivity of α-cells could control glucagon levels in patients with diabetes mellitus. The aim of this study was to investigate the preventive role of D-chiro-inositol (DCI), which has insulin receptor-sensitizer effects on insulin signaling pathways and glucagon secretion in pancreatic α-TC1 clone 6 cells. Cells were chronically treated with palmitate to induce insulin resistance in the presence/absence of DCI. DCI treatment improved the insulin signaling pathway and restored insulin-mediated glucagon suppression in α-TC1-6 cells exposed to palmitate. These results indicate that DCI treatment prevents the insulin resistance of α-TC1-6 cells chronically exposed to palmitate. Our data provide evidence that DCI could be useful to improve the insulin sensitivity of pancreatic α-cells in diabetes treatment. Full article
(This article belongs to the Special Issue Pancreatic Islets of Langerhans: Not Only Beta-Cells)
►▼ Show Figures

Figure 1

28 pages, 3716 KiB  
Article
The Constitutive Lack of α7 Nicotinic Receptor Leads to Metabolic Disorders in Mouse
by Blandine Gausserès, Junjun Liu, Ewout Foppen, Cécile Tourrel-Cuzin, Ana Rodriguez Sanchez-Archidona, Etienne Delangre, Céline Cruciani-Guglielmacci, Stéphanie Pons, Uwe Maskos, Bernard Thorens, Christophe Magnan, Jamileh Movassat and Kamel Maouche
Biomolecules 2020, 10(7), 1057; https://doi.org/10.3390/biom10071057 - 16 Jul 2020
Cited by 11 | Viewed by 3407
Abstract
Objective: Type 2 diabetes (T2D) occurs by deterioration in pancreatic β-cell function and/or progressive loss of pancreatic β-cell mass under the context of insulin resistance. α7 nicotinic acetylcholine receptor (nAChR) may contribute to insulin sensitivity but its role in the pathogenesis of T2D [...] Read more.
Objective: Type 2 diabetes (T2D) occurs by deterioration in pancreatic β-cell function and/or progressive loss of pancreatic β-cell mass under the context of insulin resistance. α7 nicotinic acetylcholine receptor (nAChR) may contribute to insulin sensitivity but its role in the pathogenesis of T2D remains undefined. We investigated whether the systemic lack of α7 nAChR was sufficient to impair glucose homeostasis. Methods: We used an α7 nAChR knock-out (α7−/−) mouse model fed a standard chow diet. The effects of the lack of α7 nAChR on islet mass, insulin secretion, glucose and insulin tolerance, body composition, and food behaviour were assessed in vivo and ex vivo experiments. Results: Young α7−/− mice display a chronic mild high glycemia combined with an impaired glucose tolerance and a marked deficit in β-cell mass. In addition to these metabolic disorders, old mice developed adipose tissue inflammation, elevated plasma free fatty acid concentrations and presented glycolytic muscle insulin resistance in old mice. Finally, α7−/− mice, fed a chow diet, exhibited a late-onset excessive gain in body weight through increased fat mass associated with higher food intake. Conclusion: Our work highlights the important role of α7 nAChR in glucose homeostasis. The constitutive lack of α7 nAChR suggests a novel pathway influencing the pathogenesis of T2D. Full article
(This article belongs to the Special Issue Pancreatic Islets of Langerhans: Not Only Beta-Cells)
►▼ Show Figures

Figure 1

Review

Jump to: Editorial, Research

19 pages, 1038 KiB  
Review
Glucagon as a Therapeutic Approach to Severe Hypoglycemia: After 100 Years, Is It Still the Antidote of Insulin?
by Francesca Porcellati, Stefania Di Mauro, Alessio Mazzieri, Alessandra Scamporrino, Agnese Filippello, Michelantonio De Fano, Carmine Giuseppe Fanelli, Francesco Purrello, Roberta Malaguarnera and Salvatore Piro
Biomolecules 2021, 11(9), 1281; https://doi.org/10.3390/biom11091281 - 27 Aug 2021
Cited by 6 | Viewed by 4679
Abstract
Hypoglycemia represents a dark and tormented side of diabetes mellitus therapy. Patients treated with insulin or drug inducing hypoglycemia, consider hypoglycemia as a harmful element, which leads to their resistance and lack of acceptance of the pathology and relative therapies. Severe hypoglycemia, in [...] Read more.
Hypoglycemia represents a dark and tormented side of diabetes mellitus therapy. Patients treated with insulin or drug inducing hypoglycemia, consider hypoglycemia as a harmful element, which leads to their resistance and lack of acceptance of the pathology and relative therapies. Severe hypoglycemia, in itself, is a risk for patients and relatives. The possibility to have novel strategies and scientific knowledge concerning hypoglycemia could represent an enormous benefit. Novel available glucagon formulations, even now, allow clinicians to deal with hypoglycemia differently with respect to past years. Novel scientific evidence leads to advances concerning physiopathological mechanisms that regulated glycemic homeostasis. In this review, we will try to show some of the important aspects of this field. Full article
(This article belongs to the Special Issue Pancreatic Islets of Langerhans: Not Only Beta-Cells)
►▼ Show Figures

Graphical abstract

23 pages, 2410 KiB  
Review
Irisin and Incretin Hormones: Similarities, Differences, and Implications in Type 2 Diabetes and Obesity
by Nicola Marrano, Giuseppina Biondi, Anna Borrelli, Angelo Cignarelli, Sebastio Perrini, Luigi Laviola, Francesco Giorgino and Annalisa Natalicchio
Biomolecules 2021, 11(2), 286; https://doi.org/10.3390/biom11020286 - 15 Feb 2021
Cited by 25 | Viewed by 6069
Abstract
Incretins are gut hormones that potentiate glucose-stimulated insulin secretion (GSIS) after meals. Glucagon-like peptide-1 (GLP-1) is the most investigated incretin hormone, synthesized mainly by L cells in the lower gut tract. GLP-1 promotes β-cell function and survival and exerts beneficial effects in different [...] Read more.
Incretins are gut hormones that potentiate glucose-stimulated insulin secretion (GSIS) after meals. Glucagon-like peptide-1 (GLP-1) is the most investigated incretin hormone, synthesized mainly by L cells in the lower gut tract. GLP-1 promotes β-cell function and survival and exerts beneficial effects in different organs and tissues. Irisin, a myokine released in response to a high-fat diet and exercise, enhances GSIS. Similar to GLP-1, irisin augments insulin biosynthesis and promotes accrual of β-cell functional mass. In addition, irisin and GLP-1 share comparable pleiotropic effects and activate similar intracellular pathways. The insulinotropic and extra-pancreatic effects of GLP-1 are reduced in type 2 diabetes (T2D) patients but preserved at pharmacological doses. GLP-1 receptor agonists (GLP-1RAs) are therefore among the most widely used antidiabetes drugs, also considered for their cardiovascular benefits and ability to promote weight loss. Irisin levels are lower in T2D patients, and in diabetic and/or obese animal models irisin administration improves glycemic control and promotes weight loss. Interestingly, recent evidence suggests that both GLP-1 and irisin are also synthesized within the pancreatic islets, in α- and β-cells, respectively. This review aims to describe the similarities between GLP-1 and irisin and to propose a new potential axis–involving the gut, muscle, and endocrine pancreas that controls energy homeostasis. Full article
(This article belongs to the Special Issue Pancreatic Islets of Langerhans: Not Only Beta-Cells)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-8
Back to TopTop