scholarly journals Extracellularly Regulated Kinases 1/2 (p44/42 Mitogen-Activated Protein Kinases) Phosphorylate Synapsin I and Regulate Insulin Secretion in the MIN6 β-Cell Line and Islets of Langerhans

Endocrinology ◽  
2005 ◽  
Vol 146 (2) ◽  
pp. 643-654 ◽  
Author(s):  
Christine Longuet ◽  
Christophe Broca ◽  
Safia Costes ◽  
El Habib Hani ◽  
Dominique Bataille ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Cell Line ◽  
Protein Kinases ◽  
Islets Of Langerhans ◽  
Synapsin I ◽  
Β Cell ◽  
Mitogen Activated Protein Kinases ◽  
Mitogen Activated Protein

scholarly journals Perilipin Is Present in Islets of Langerhans and Protects against Lipotoxicity When Overexpressed in the β-Cell Line INS-1

Endocrinology ◽  
2009 ◽  
Vol 150 (7) ◽  
pp. 3049-3057 ◽  
Author(s):  
Jörgen Borg ◽  
Cecilia Klint ◽  
Nils Wierup ◽  
Kristoffer Ström ◽  
Sara Larsson ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Cell Line ◽  
Islets Of Langerhans ◽  
Prolonged Exposure ◽  
Human Islets ◽  
Lipid Storage ◽  
Β Cells ◽  
Β Cell ◽  
Glucose Stimulated Insulin Secretion ◽  
In Cells

Lipids have been shown to play a dual role in pancreatic β-cells: a lipid-derived signal appears to be necessary for glucose-stimulated insulin secretion, whereas lipid accumulation causes impaired insulin secretion and apoptosis. The ability of the protein perilipin to regulate lipolysis prompted an investigation of the presence of perilipin in the islets of Langerhans. In this study evidence is presented for perilipin expression in rat, mouse, and human islets of Langerhans as well as the rat clonal β-cell line INS-1. In rat and mouse islets, perilipin was verified to be present in β-cells. To examine whether the development of lipotoxicity could be prevented by manipulating the conditions for lipid storage in the β-cell, INS-1 cells with adenoviral-mediated overexpression of perilipin were exposed to lipotoxic conditions for 72 h. In cells exposed to palmitate, perilipin overexpression caused increased accumulation of triacylglycerols and decreased lipolysis compared with control cells. Whereas glucose-stimulated insulin secretion was retained after palmitate exposure in cells overexpressing perilipin, it was completely abolished in control β-cells. Thus, overexpression of perilipin appears to confer protection against the development of β-cell dysfunction after prolonged exposure to palmitate by promoting lipid storage and limiting lipolysis.

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