Journal
INTERNATIONAL JOURNAL OF FOOD SCIENCES AND NUTRITION
Volume 68, Issue 4, Pages 455-466Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/09637486.2016.1261086
Keywords
Obesity; developmental programming; NAFLD; ER stress; circadian rhythm
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Funding
- Welcome Trust
- Obesity Action Campaign
- Fiorina Elliot Charity grant (from the Royal Free Charity)
- BBSRC [BB/H008845/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/H008845/1] Funding Source: researchfish
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We investigated the regulation of hepatic ER stress in healthy liver and adult or perinatally programmed diet-induced non-alcoholic fatty liver disease (NAFLD). Female mice were fed either obesogenic or control diet before mating, during pregnancy and lactation. Post-weaning, offspring from each maternal group were divided into either obesogenic or control diet. At six months, offspring were sacrificed at 4-h intervals over 24h. Offspring fed obesogenic diets developed NAFLD phenotype, and the combination of maternal and offspring obesogenic diets exacerbated this phenotype. UPR signalling pathways (IREa, PERK, ATF6) and their downstream regulators showed different basal rhythmicity, which was modified in offspring exposed to obesogenic diet and maternal programming. The double obesogenic hit increased liver apoptosis measured by TUNEL staining, active caspase-3 and phospho-JNK and GRP78 promoter methylation levels. This study demonstrates that hepatic UPR is rhythmically activated. The combination of maternal obesity (MO) and obesogenic diets in offspring triggered altered UPR rhythmicity, DNA methylation and cellular apoptosis.
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