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Perilipin is present in islets of Langerhans and protects against lipotoxicity when overexpressed in the beta-cell line INS-1.

Borg, Jörgen LU ; Klint, Cecilia LU ; Wierup, Nils LU ; Ström, Kristoffer LU ; Larsson, Sara LU ; Sundler, Frank LU ; Lupi, Roberto; Marchetti, Piero; Xu, Guoheng and Kimmel, Alan, et al. (2009) In Endocrinology 150(7). p.3049-3057
Abstract
Lipids have been shown to play a dual role in pancreatic beta-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 in the rat clonal beta-cell line INS-1. In rat and mouse islets, perilipin was verified to be present in beta-cells. In order to examine if the development of lipotoxicity could be prevented by manipulating the conditions for lipid storage in the... (More)
Lipids have been shown to play a dual role in pancreatic beta-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 in the rat clonal beta-cell line INS-1. In rat and mouse islets, perilipin was verified to be present in beta-cells. In order to examine if the development of lipotoxicity could be prevented by manipulating the conditions for lipid storage in the beta-cell, INS-1 cells with adenoviral-mediated overexpression of perilipin were exposed to lipotoxic conditions for 72 hours. In cells exposed to palmitate, perilipin overexpression caused increased accumulation of triacylglycerols and decreased lipolysis compared to control cells. Whereas glucose-stimulated insulin secretion was retained following palmitate exposure in cells overexpressing perilipin, it was completely abolished in control beta-cells. Thus, overexpression of perilipin appears to confer protection against the development of beta-cell dysfunction following prolonged exposure to palmitate by promoting lipid storage and limiting lipolysis. (Less)
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Contribution to journal
publication status
published
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Endocrinology
volume
150
issue
7
pages
3049 - 3057
publisher
Endocrine Society
external identifiers
  • wos:000267781300011
  • pmid:19299455
  • scopus:67649646763
ISSN
0013-7227
DOI
10.1210/en.2008-0913
language
English
LU publication?
yes
id
c0fdc3af-bc3a-4c35-8586-5f181c7957be (old id 1367613)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/19299455?dopt=Abstract
date added to LUP
2009-04-07 15:01:52
date last changed
2017-08-13 03:47:30
@article{c0fdc3af-bc3a-4c35-8586-5f181c7957be,
  abstract     = {Lipids have been shown to play a dual role in pancreatic beta-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 in the rat clonal beta-cell line INS-1. In rat and mouse islets, perilipin was verified to be present in beta-cells. In order to examine if the development of lipotoxicity could be prevented by manipulating the conditions for lipid storage in the beta-cell, INS-1 cells with adenoviral-mediated overexpression of perilipin were exposed to lipotoxic conditions for 72 hours. In cells exposed to palmitate, perilipin overexpression caused increased accumulation of triacylglycerols and decreased lipolysis compared to control cells. Whereas glucose-stimulated insulin secretion was retained following palmitate exposure in cells overexpressing perilipin, it was completely abolished in control beta-cells. Thus, overexpression of perilipin appears to confer protection against the development of beta-cell dysfunction following prolonged exposure to palmitate by promoting lipid storage and limiting lipolysis.},
  author       = {Borg, Jörgen and Klint, Cecilia and Wierup, Nils and Ström, Kristoffer and Larsson, Sara and Sundler, Frank and Lupi, Roberto and Marchetti, Piero and Xu, Guoheng and Kimmel, Alan and Londos, Constantine and Holm, Cecilia},
  issn         = {0013-7227},
  language     = {eng},
  number       = {7},
  pages        = {3049--3057},
  publisher    = {Endocrine Society},
  series       = {Endocrinology},
  title        = {Perilipin is present in islets of Langerhans and protects against lipotoxicity when overexpressed in the beta-cell line INS-1.},
  url          = {http://dx.doi.org/10.1210/en.2008-0913},
  volume       = {150},
  year         = {2009},
}