UPR in palmitate-treated pancreatic beta-cells is not affected by altering oxidation of the fatty acid

Elevated levels of lipids are detrimental for beta-cell function and mass. One of the mechanisms of how fatty acids induce apoptosis is development of the unfolded protein response (UPR). It is still far from understood how fatty acids activate the UPR, however. We examined how palmitate-induced act...

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Bibliographic Details
Published in:Nutrition & metabolism 2011-10, Vol.8 (1), p.70-366
Main Authors: Sargsyan, Ernest, Sol, E-Ri Maria, Bergsten, Peter
Format: Article
Language:English
Subjects:
Apoptosis
beta-cell
ER stress
Experiments
fatty acid metabolism
Fatty acids
glucose
human cell lines
human islets
Kinases
oxidation
palmitate oxidation
Phosphorylation
Protein synthesis
Stress response
Studies
unfolded protein response
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Summary:Elevated levels of lipids are detrimental for beta-cell function and mass. One of the mechanisms of how fatty acids induce apoptosis is development of the unfolded protein response (UPR). It is still far from understood how fatty acids activate the UPR, however. We examined how palmitate-induced activation of the UPR was affected by altering the metabolism of the fatty acid in insulin-secreting INS-1E and MIN6 cell lines and intact human islets. To increase oxidation, we used low glucose (5.5 mM) or AICAR; and to reduce oxidation, we used high glucose (25 mM) or etomoxir. UPR was measured after 3, 24 and 48 hours of palmitate treatment. Modulation of palmitate oxidation by either glucose or the pharmacological agents did not affect palmitate-induced UPR activation. Our finding suggests that other factors than oxidation of palmitate play a role in the activation of UPR in fatty acid-treated beta-cells.
ISSN:1743-7075
1743-7075
DOI:10.1186/1743-7075-8-70