Figure 4
From: Caspase-2 promotes obesity, the metabolic syndrome and nonalcoholic fatty liver disease
Adipose tissue from caspase-2-deficient mice is resistant to energy surplus induced apoptosis. (a) Adipose tissue UCP (qRT-PCR, immunoblot). (b) Cleaved caspase-3 expression in adipose tissue (immunoblot). All animals were evaluated (four animals per genotype in chow diet groups and eight animals per genotype in Western diet groups), at sacrifice. The errors reported represent mean±S.E.M., normalized to chow-diet-fed WT mice. *P<0.05, **P<0.01 chow versus Western diet; #P<0.05, ##P<0.01 WT versus knockout mice. (c) Right panel: oil red staining demonstrating 3T3-L1 cell differentiation into adipocytes. Scale bar, 500 μm. Middle panel: caspase-3/7 activity (measured by luminescence, normalized to number of viable cells assessed by fluorescence, according to manufacturer instructions) in adipocytes treated with palmitate (1 mM)±caspase-2 inhibitor (20 uM). Left panel: cytotoxicity assay in the same wells as apoptosis assay. *P<0.05 and **P<0.01 palmitate versus control treated cells; ##P<0.01 cells treated with caspase-2 inhibitor versus no treatment
