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UPR in palmitate-treated pancreatic beta-cells is not affected by altering oxidation of the fatty acid
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
2011 (English)In: Nutrition & Metabolism, ISSN 1743-7075, E-ISSN 1743-7075, Vol. 8, p. 70-Article in journal (Refereed) Published
Abstract [en]

Background: 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.

Methods: 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.

Results: Modulation of palmitate oxidation by either glucose or the pharmacological agents did not affect palmitate-induced UPR activation.

Conclusion: Our finding suggests that other factors than oxidation of palmitate play a role in the activation of UPR in fatty acid-treated beta-cells.

Place, publisher, year, edition, pages
2011. Vol. 8, p. 70-
Keyword [en]
beta-cell, human islets, palmitate oxidation, ER stress, unfolded protein response
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-162371DOI: 10.1186/1743-7075-8-70ISI: 000296718700001OAI: oai:DiVA.org:uu-162371DiVA: diva2:460505
Available from: 2011-11-30 Created: 2011-11-30 Last updated: 2017-12-08Bibliographically approved

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