Fig. 4.

ERα deletion causes reduced skeletal muscle fatty acid oxidation, accumulation of bioactive lipid intermediates, and inflammation during NC feeding. IB, RT-PCR, and biochemical analyses were performed on quadriceps muscle harvested from WT (open bars) and ERα-KO (black bars) mice (n = 6–12 animals/genotype). A: IB and densitometric analyses for phospho-AMP-activated protein kinase (p-AMPK). RT-PCR analyses were performed to quantify peroxisome proliferator-activated receptor (PPAR)α and PPARδ (B) as well as uncoupling protein-2 (UCP2) and sterol regulatory element-binding protein-1c (SREBP-1c) expression levels (C). Muscle lipid and lipid intermediates, ceramide (D), diacylglycerol, (E) and triacylglycerol (F) were quantified by biochemical assay. IB and RT-PCR analyses were performed to assess inflammatory signaling in quadriceps muscle: p-JNK (G) and TNFα/GAPDH mRNA (H) expression. Densitometric and RT-PCR analyses are presented as means ± SE in AU. Mean differences between WT vs. KO mice were detected using ANOVA. *P < 0.05.