Beta cell failure is caused by loss of cell mass, mostly by apoptosis, but also by simple dysfunction (decline of glucose-stimulated insulin secretion, downregulation of specific gene expression). Apoptosis and dysfunction are caused, at least in part, by lipoglucotoxicity. The mechanisms implicated are oxidative stress, increase in the hexosamine biosynthetic pathway (HBP) flux and endoplasmic reticulum (ER) stress. Oxidative stress plays a role in glucotoxicity-induced beta cell dedifferentiation, while glucotoxicity-induced ER stress has been mostly linked to beta cell apoptosis. We sought to clarify whether ER stress caused by increased HBP flux participates in a dedifferentiating response of beta cells, in the absence of relevant apoptosis.

Increased hexosamine biosynthetic pathway flux dedifferentiates INS-1E cells and murine islets by an extracellular signal-regulated kinase (ERK)1/2-mediated signal transmission pathway / Lombardi, A; Ulianich, Luca; Treglia, A. S; Nigro, Cecilia; Parrillo, Luca; Lofrumento, D. D; Nicolardi, Federica; Garbi, Corrado; Beguinot, Francesco; Miele, Claudia; DI JESO, Bruno. - In: DIABETOLOGIA. - ISSN 0012-186X. - 55:1(2012), pp. 141-153. [10.1007/s00125-011-2315-1]

Increased hexosamine biosynthetic pathway flux dedifferentiates INS-1E cells and murine islets by an extracellular signal-regulated kinase (ERK)1/2-mediated signal transmission pathway

GARBI, CORRADO;BEGUINOT, FRANCESCO;
2012

Abstract

Beta cell failure is caused by loss of cell mass, mostly by apoptosis, but also by simple dysfunction (decline of glucose-stimulated insulin secretion, downregulation of specific gene expression). Apoptosis and dysfunction are caused, at least in part, by lipoglucotoxicity. The mechanisms implicated are oxidative stress, increase in the hexosamine biosynthetic pathway (HBP) flux and endoplasmic reticulum (ER) stress. Oxidative stress plays a role in glucotoxicity-induced beta cell dedifferentiation, while glucotoxicity-induced ER stress has been mostly linked to beta cell apoptosis. We sought to clarify whether ER stress caused by increased HBP flux participates in a dedifferentiating response of beta cells, in the absence of relevant apoptosis.
2012
Increased hexosamine biosynthetic pathway flux dedifferentiates INS-1E cells and murine islets by an extracellular signal-regulated kinase (ERK)1/2-mediated signal transmission pathway / Lombardi, A; Ulianich, Luca; Treglia, A. S; Nigro, Cecilia; Parrillo, Luca; Lofrumento, D. D; Nicolardi, Federica; Garbi, Corrado; Beguinot, Francesco; Miele, Claudia; DI JESO, Bruno. - In: DIABETOLOGIA. - ISSN 0012-186X. - 55:1(2012), pp. 141-153. [10.1007/s00125-011-2315-1]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11588/671899
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