Altered cellular redox status, sirtuin abundance and clock gene expression in a mouse model of developmentally primed NASH
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- 作者：Kimberley D. Brucea ; b ; Kimberley.bruce@ucdenver.edu" class="auth_mail" title="E-mail the corresponding author ; Dawid Szczepankiewiczc ; Kiran K. Sihotaa ; Manoj Ravindraanandana ; Hugh Thomasa ; Karen A. Lillycropd ; Graham C. Burdgea ; Mark A. Hansona ; Christopher D. Byrnea ; Felino R. Cagampanga
- 关键词：NAFLD ; non-alcoholic fatty liver disease ; NASH ; non-alcoholic steatohepatitis ; HF ; high fat ; C ; control ; sirt1 ; sirtuin 1 ; sirt3 ; sirtuin 3 ; Clock ; circadian locomotor output cycles kaput ; Per2 ; Bmal1 (also called Arntl1) ; period 2 ; Cry2 ; cryptochrome 2 ; RORα ; retinoic acid receptor-related orphan receptor alpha ; Srebp1c ; sterol regulatory element binding protein-1c ; NAD ; nicotinamide adenine dinucleotide ; OPN ; osteopontin
- 刊名：Biochimica et Biophysica Acta (BBA)-Molecular and Cell Biology of Lipids
- 出版年：2016
- 出版时间：July 2016
- 年：2016
- 卷：1861
- 期：7
- 页码：584-593
- 全文大小：1082 K
文摘
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Offspring of mothers fed a high fat diet show severe fatty liver in later life.
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HF feeding is associated with altered cellular redox status and reduced sirtuin gene expression.
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HF feeding desynchronises the expression of core clock genes and lipogenic transcription factors.
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Exposure to a HF diet during development causes changes in liver metabolism that precede severe fatty liver disease.