A Predominant Role for Parenchymal c-Jun Amino Terminal Kinase (JNK) in the Regulation of Systemic Insulin Sensitivity (original) (raw)
Figure 8
Hepatic triglyceride accumulation and inflammatory cytokines expression in the liver and subcutaneous adipose tissue.
Photomicrographs of liver sections were generated after staining with hematoxylin/eosin. Liver sections were prepared from all groups of mice, Jnk1−/−_→_WT, WT→WT, WT_→_Jnk1−/− and Jnk1−/−_→_Jnk1−/−, on high-fat diet for 27 weeks (A). In the same liver samples, triglycerides were extracted and quantified (B). Additionally, total RNA was extracted and expression levels of IL-1β, IL-6, TNF-α, and F4/80 were quantified to determine the cellular milieu in the WT (C) or Jnk1−/− (D) recipient groups transplanted with WT or Jnk1−/− bone marrow. Similarly, mRNA was extracted from subcutaneous adipose tissue in the WT (E) or Jnk1−/− (F) recipient groups and subjected to quantitative-PCR analysis of the IL-1β, IL-6, TNF-α, and F4/80 expression. Asterisk indicates statistical significance (p<0.05) in Student's t test.