Characterization of β-cell plasticity mechanisms induced in mice by a transient source of exogenous insulin.

Détails

ID Serval
serval:BIB_8E42FCE3C719
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Characterization of β-cell plasticity mechanisms induced in mice by a transient source of exogenous insulin.
Périodique
American Journal of Physiology. Endocrinology and Metabolism
Auteur(s)
Nollevaux M.C., Rahier J., Marchandise J., Thurion P., Godecharles S., Van den Steen G., Jamart J., Sempoux C., Jacquemin P., Guiot Y.
ISSN
1522-1555 (Electronic)
ISSN-L
0193-1849
Statut éditorial
Publié
Date de publication
2013
Volume
304
Numéro
7
Pages
E711-E723
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov'tPublication Status: ppublish
Résumé
β-Cell plasticity governs the adjustment of β-cell mass and function to ensure normoglycemia. The study of how β-cell mass is controlled and the identification of alternative sources of β-cells are active fields of research. β-Cell plasticity has been implicated in numerous physiological and pathological conditions. We developed a mice model in which we induced major β-cell mass atrophy by implanting insulin pellets (IPI) for 7 or 10 days. The implants were then removed (IPR) to observe the timing and characteristics of β-cell regeneration in parallel to changes in glycemia. Following IPR, the endocrine mass was reduced by 60% at day 7 and by 75% at day 10, and transient hyperglycemia was observed, which resolved within 1 wk. Five days after IPR, enhanced β-cell proliferation and an increased frequency of small islets were observed in 7-day IPI mice. β-Cell mass was fully restored after an additional 2 days. For the 10-day IPI group, β-cell and endocrine mass were no longer significantly different from those of the control group at 2 wk post-IPR. Furthermore, real-time quantitative PCR analysis of endocrine structures isolated by laser capture microdissection indicated sequentially enhanced expression of the pancreatic transcription factors β(2)/NeuroD and Pdx-1 post-IPR. Thus, our data suggest this mouse model of β-cell plasticity not only relies on replication but also involves enhanced cell differentiation plasticity.
Mots-clé
Animals, Apoptosis/drug effects, Apoptosis/physiology, Cell Enlargement/drug effects, Cell Proliferation, Congenital Hyperinsulinism, Female, Glucose/metabolism, Glucose Transporter Type 2/metabolism, Hypoglycemia/chemically induced, Hypoglycemic Agents/pharmacology, Insulin/pharmacology, Insulin-Secreting Cells/drug effects, Insulin-Secreting Cells/pathology, Islets of Langerhans/cytology, Islets of Langerhans/drug effects, Laser Capture Microdissection, Mice, Nesidioblastosis, Polymerase Chain Reaction, RNA, Messenger/analysis, Regeneration/drug effects, Regeneration/physiology, Time Factors, Transcription Factors/metabolism
Pubmed
Web of science
Création de la notice
26/01/2015 12:32
Dernière modification de la notice
03/03/2018 19:18
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