Maternal obesity alters endoplasmic reticulum homeostasis in offspring pancreas
XBP1
ATF6
DOI:
10.1007/s13105-016-0476-6
Publication Date:
2016-03-18T17:14:28Z
AUTHORS (12)
ABSTRACT
The prevalence of non-alcoholic fatty pancreas disease (NAFPD) is increasing in parallel with obesity rates. Stress-related alterations endoplasmic reticulum (ER), such as the unfolded protein response (UPR), are associated obesity. aim this study was to investigate ER imbalance a mice model adult and perinatal diet-induced Twenty female C57BL/6J were assigned control (Con) or obesogenic (Ob) diets prior during pregnancy lactation. Their offspring weaned onto Con Ob up 6 months post-partum. Then, after sacrifice, plasma biochemical analyses, gene expression, concentrations measured pancreata. Offspring Ob-fed had significantly increased body weight (p < 0.001) leptin decreased insulin 0.01) levels. Maternal diet total phosphorylated Eif2α spliced X-box binding 1 (XBP1). Pancreatic expression downstream regulators UPR (EDEM, homocysteine-responsive reticulum-resident (HERP), activating transcription factor 4 (ATF4), C/EBP homologous (CHOP)) autophagy-related proteins (LC3BI/LC3BII) differently disrupted by feeding both mothers (from p 0.1 0.001). their alter NAFPD, involvement proapoptotic markers. Upstream PERK, IRE1α, ATF6 pathways affected following insults.
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