Pancreatic islet of Langerhans' cytoarchitecture and ultrastructure in normal glucose tolerance and in type 2 diabetes mellitus.

Détails

ID Serval
serval:BIB_A1FCDD1F1A99
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Titre
Pancreatic islet of Langerhans' cytoarchitecture and ultrastructure in normal glucose tolerance and in type 2 diabetes mellitus.
Périodique
Diabetes, obesity & metabolism
Auteur(s)
Folli F., La Rosa S., Finzi G., Davalli A.M., Galli A., Dick E.J., Perego C., Mendoza R.G.
ISSN
1463-1326 (Electronic)
ISSN-L
1462-8902
Statut éditorial
Publié
Date de publication
09/2018
Peer-reviewed
Oui
Volume
20 Suppl 2
Pages
137-144
Langue
anglais
Notes
Publication types: Journal Article ; Review
Publication Status: ppublish
Résumé
While a number of structural and cellular abnormalities occur in the islet of Langerhans in diabetes, and in particular in type 2 diabetes, the focus has been mostly on the insulin producing β-cells and only more recently on glucagon producing α- and δ-cells. There is ample evidence that in type 2 diabetes mellitus (T2DM), in addition to a progressive decline in β-cell function and associated insulin resistance in a number of insulin-sensitive tissues, alterations in glucagon secretion are also present and may play an important role in the pathogenesis of hyperglycemia both in the fasting and in the postprandial state. Recently, a number of studies have showed that there are also functional and structural alterations in glucagon-producing α-cells and somatostatin-producing δ-cells. Thus, it is becoming increasingly clear that multiple cellular alterations of multiple cell types occur, which adds even more complexity to our understanding of the pathophysiology of this common and severe disease. We believe that persistent efforts to increase the understanding of the pathophysiology of hormone secretion in the islets of Langerhans will also improve our capability to better prevent and treat diabetes mellitus.
Mots-clé
Amyloid/metabolism, Animals, Blood Glucose/metabolism, Diabetes Mellitus, Type 2/pathology, Glucagon-Secreting Cells/ultrastructure, Haplorhini, Humans, Islets of Langerhans/cytology, Islets of Langerhans/ultrastructure, Mice, Models, Animal, Pancreatic Polypeptide-Secreting Cells/ultrastructure, Papio, Rats, Somatostatin-Secreting Cells/ultrastructure, IAPP, amyloid deposition, electron microscopy insulin producing β-cells, glucagon producing α-cells, pancreatic islet of Langerhans structure, somatostatin producing δ-cells, type 2 diabetes mellitus, ultrastructure
Pubmed
Web of science
Open Access
Oui
Création de la notice
21/09/2018 9:42
Dernière modification de la notice
20/08/2019 15:08
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