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Open Access Research

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

Ernest Sargsyan*, E-ri Maria Sol and Peter Bergsten

Author Affiliations

Department of Medical Cell Biology, Uppsala University, Box 571, SE-75123, Uppsala, Sweden

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Nutrition & Metabolism 2011, 8:70  doi:10.1186/1743-7075-8-70

Published: 6 October 2011

Abstract

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.

Keywords:
beta-cell; human islets; palmitate oxidation; ER stress; unfolded protein response