Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/28505
Title: ER stress in rodent islets of Langerhans is concomitant with obesity and β-cell compensation but not with β-cell dysfunction and diabetes
Authors: Omikorede, O.
Qi, C.
Gorman, T.
Chapman, P.
Yu, A.
Smith, D.M.
Herbert, Terence P.
First Published: 21-Oct-2013
Publisher: Nature Publishing Group
Citation: Nutrition and Diabetes, 2013, 3, e93
Abstract: Objective: The objective of this study was to determine whether ER stress correlates with b-cell dysfunction in obesity-associated diabetes. Methods: Quantitative RT-PCR and western blot analysis were used to investigate changes in the expression of markers of ER stress, the unfolded protein response (UPR) and β-cell function in islets isolated from (1) non-diabetic Zucker obese (ZO) and obese female Zucker diabetic fatty (fZDF) rats compared with their lean littermates and from (2) high-fat-diet-fed fZDF rats (HF-fZDF), to induce diabetes, compared with age-matched non-diabetic obese fZDF rats. Results: Markers of an adaptive ER stress/UPR and β-cell function are elevated in islets isolated from ZO and fZDF rats compared with their lean littermates. In islets isolated from HF-fZDF rats, there was no significant change in the expression of markers of ER stress compared with age matched, obese, non-diabetic fZDF rats. Conclusions: These results provide evidence that obesity-induced activation of the UPR is an adaptive response for increasing the ER folding capacity to meet the increased demand for insulin. As ER stress is not exacerbated in high-fat-diet-induced diabetes, we suggest that failure of the islet to mount an effective adaptive UPR in response to an additional increase in insulin demand, rather than chronic ER stress, may ultimately lead to β-cell failure and hence diabetes.
DOI Link: 10.1038/nutd.2013.35
eISSN: 2044-4052
Links: http://www.nature.com/nutd/journal/v3/n10/full/nutd201335a.html
http://hdl.handle.net/2381/28505
Version: Publisher Version
Status: Peer-reviewed
Type: Journal Article
Rights: Copyright © 2013 Macmillan Publishers Limited. This work is licensed under a Creative Commons Attribution 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by/3.0/.
Appears in Collections:Published Articles, Dept. of Cell Physiology and Pharmacology

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