ijms-logo

Journal Browser

Journal Browser

The Biology and Pharmacology of Glucagon 2.0

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

Deadline for manuscript submissions: closed (15 July 2022) | Viewed by 5707

Special Issue Editor


E-Mail Website
Guest Editor
Division of Diabetes and Metabolism, Nihon University School of Medicine, Itabashi, Tokyo 173-8610, Japan
Interests: insulin secretion; beta-cell; glucagon secretion; islet of Langerhans; SGLT2 inhibitor; GLP-1RA; cell replacement therapy; metabolic reprogramming

Special Issue Information

Dear Colleagues,

The discovery of insulin and its pharmacology in 1921 was closely followed by that of glucagon in 1923. However, unlike insulin, glucagon action has been historically stigmatized as diabetogenic and its clinical use restricted to rescue from severe hypoglycemia. Hampered by a short half-life and poor solubility in physiological buffers, this glucocentric view of glucagon has overshadowed that glucagon is a pleiotropic hormone with broad biological action not only in the pancreas and the liver but also in the brain, the heart, the stomach and the white and brown adipose tissue. The diabetogenic reputation of glucagon is urged by reports showing that failure of glucose to suppress glucagon secretion can play a pathophysiological role in the development of type 2 diabetes, while blockade of glucagon can ameliorate hyperglycemia in diabetic patients. Ironically, the diabetogenic view of glucagon has recently been challenged by the generation of pharmacotherapies that along with insulinotropic peptides recruit glucagon receptor agonism into the same entity to treat obesity and type 2 diabetes.

In this Special Issue, we describe the multifaceted nature of glucagon that goes well beyond its role on glucose metabolism. Both original research articles and comprehensive reviews are welcomed.

Prof. Dr. Hisamitsu Ishihara
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

  • glucagon
  • GCGR
  • glucagon receptor
  • GLP-1
  • GLP-1R
  • diabetes
  • obesity
  • insulin

Published Papers (1 paper)

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

Review

19 pages, 1010 KiB  
Review
The Role of the α Cell in the Pathogenesis of Diabetes: A World beyond the Mirror
by María Sofía Martínez, Alexander Manzano, Luis Carlos Olivar, Manuel Nava, Juan Salazar, Luis D’Marco, Rina Ortiz, Maricarmen Chacín, Marion Guerrero-Wyss, Mayela Cabrera de Bravo, Clímaco Cano, Valmore Bermúdez and Lisse Angarita
Int. J. Mol. Sci. 2021, 22(17), 9504; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22179504 - 01 Sep 2021
Cited by 13 | Viewed by 5128
Abstract
Type 2 Diabetes Mellitus (T2DM) is one of the most prevalent chronic metabolic disorders, and insulin has been placed at the epicentre of its pathophysiological basis. However, the involvement of impaired alpha (α) cell function has been recognized as playing an essential role [...] Read more.
Type 2 Diabetes Mellitus (T2DM) is one of the most prevalent chronic metabolic disorders, and insulin has been placed at the epicentre of its pathophysiological basis. However, the involvement of impaired alpha (α) cell function has been recognized as playing an essential role in several diseases, since hyperglucagonemia has been evidenced in both Type 1 and T2DM. This phenomenon has been attributed to intra-islet defects, like modifications in pancreatic α cell mass or dysfunction in glucagon’s secretion. Emerging evidence has shown that chronic hyperglycaemia provokes changes in the Langerhans’ islets cytoarchitecture, including α cell hyperplasia, pancreatic beta (β) cell dedifferentiation into glucagon-positive producing cells, and loss of paracrine and endocrine regulation due to β cell mass loss. Other abnormalities like α cell insulin resistance, sensor machinery dysfunction, or paradoxical ATP-sensitive potassium channels (KATP) opening have also been linked to glucagon hypersecretion. Recent clinical trials in phases 1 or 2 have shown new molecules with glucagon-antagonist properties with considerable effectiveness and acceptable safety profiles. Glucagon-like peptide-1 (GLP-1) agonists and Dipeptidyl Peptidase-4 inhibitors (DPP-4 inhibitors) have been shown to decrease glucagon secretion in T2DM, and their possible therapeutic role in T1DM means they are attractive as an insulin-adjuvant therapy. Full article
(This article belongs to the Special Issue The Biology and Pharmacology of Glucagon 2.0)
Show Figures

Figure 1

Back to TopTop