Research Paper Volume 12, Issue 19 pp 19677—19700

High fat diet can specifically protect the liver from impaired mitochondrial biogenesis by upregulating a transcriptional stress response. (A) Liver sections cut to 10-μm thickness were stained with H&E, from NCD or HFD fed Ptcd1^+/+ (n=5) and Ptcd1^+/- (n=5) mice. (B) Liver sections cut to 10 μm thickness were stained with Oil red O and hematoxylin, from NCD or HFD fed 17-week-old Ptcd1^+/+ (n=5) and Ptcd1^+/- (n=5) mice. (C) White adipose tissue sections cut to 5-μm thickness were stained with H&E, from 17-week-old Ptcd1^+/+ (n=5) and Ptcd1^+/- (n=5) mice fed either a NCD or HFD. (D) Skeletal muscle tissue sections cut to 5-μm thickness were stained with H&E, from Ptcd1^+/+ (n=5) and Ptcd1^+/- (n=5) mice fed either a NCD or HFD. Scale bars are 100 μm. (E) Triacylglycerol levels were measured in total liver and skeletal muscle isolated from NCD and HFD Ptcd1^+/+ (n=9) and Ptcd1^+/- (n=9) mice. Mitochondrial transcription factor mRNAs Atf4, Atf5 and Chop were measured in total liver (F) and skeletal muscle RNA isolated from NCD and HFD Ptcd1^+/+ (n=5) and Ptcd1^+/- (n=5) mice by qRT-PCR and normalized to 18S rRNA. (G) Endogenous levels of SAPK/JNK and its phosphorylated form (Thr¹⁸³/Tyr¹⁸⁵) were determined by immunoblotting of whole tissue lysates from skeletal muscle and livers of 17-week-old Ptcd1^+/+ (n=5) and Ptcd1^+/- mice (n=5) fed a NCD or HFD. GAPDH (glyceraldehyde-3-phosphate dehydrogenase) was used as a loading control. Relative protein levels and relative intensity percentage of phosphorylation versus total protein levels were measured using ImageJ software and normalized to GAPDH. Error bars are SEM. *P < 0.05, ***P<0.001, Student’s t test.