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Journal of Physiology and Biochemistry

, Volume 72, Issue 2, pp 281–291

First Online: 15 March 2016Received: 07 December 2015Accepted: 29 February 2016DOI: 10.1007-s13105-016-0476-6

Cite this article as: Soeda, J., Mouralidarane, A., Cordero, P. et al. J Physiol Biochem 2016 72: 281. doi:10.1007-s13105-016-0476-6

Abstract

The prevalence of non-alcoholic fatty pancreas disease NAFPD is increasing in parallel with obesity rates. Stress-related alterations in endoplasmic reticulum ER, such as the unfolded protein response UPR, are associated with obesity. The aim of this study was to investigate ER imbalance in the pancreas of a mice model of adult and perinatal diet-induced obesity. Twenty female C57BL-6J mice were assigned to control Con or obesogenic Ob diets prior to and during pregnancy and lactation. Their offspring were weaned onto Con or Ob diets up to 6 months post-partum. Then, after sacrifice, plasma biochemical analyses, gene expression, and protein concentrations were measured in pancreata. Offspring of Ob-fed mice had significantly increased body weight p < 0.001 and plasma leptin p < 0.001 and decreased insulin p < 0.01 levels. Maternal obesogenic diet decreased the total and phosphorylated Eif2α and increased spliced X-box binding protein 1 XBP1. Pancreatic gene expression of downstream regulators of UPR EDEM, homocysteine-responsive endoplasmic reticulum-resident HERP, activating transcription factor 4 ATF4, and C-EBP homologous protein CHOP and autophagy-related proteins LC3BI-LC3BII were differently disrupted by obesogenic feeding in both mothers and offspring from p < 0.1 to p < 0.001. Maternal obesity and Ob feeding in their offspring alter UPR in NAFPD, with involvement of proapoptotic and autophagy-related markers. Upstream and downstream regulators of PERK, IRE1α, and ATF6 pathways were affected differently following the obesogenic insults.

KeywordsFatty pancreas Obesity Perinatal programming ER stress UPR Autophagy  Download fulltext PDF



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