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. Author manuscript; available in PMC: 2011 Dec 22.
Published in final edited form as: Nat Med. 2011 Aug 21;17(9):1076–1085. doi: 10.1038/nm.2439

Figure 4.

Figure 4

Changes in PPAR-α and PPAR-δ activated gene expression and OXPHOS in mice lacking or overexpressing Atgl in cardiac muscle. (a) Cardiac triglyceride content in wild-type and conditional knockout mice lacking Atgl in cardiac and skeletal muscle (muscleAtg/KO mice) demonstrating a drastic cardiac steatosis in muscleAtg/KO mice (n = 5). Scale bars, 5 mm. (b) mRNA expression levels of PPAR-α and PPAR-δ target genes and of the gene encoding PGC-1α in cardiac muscle of muscleAtg/KO mice compared to wild-type mice (n = 5). (c–e) Heart weight (c), cardiac muscle triglyceride (TG) content (d), and white and brown adipose tissue (WAT and BAT) weight (e) of wild-type, Atg/KO and Atg/KO-cmAtg/TG mice expressing an Atgl transgene on an Atg/KO background (n = 6). (f) mRNA expression levels of PPAR-α and PPAR-δ target genes and genes encoding PGC-1α and PGC-1β in cardiac muscle of wild-type, Atg/KO and Atg/KO-cmAtg/TG mice (n = 4). (g) Oxygen consumption in cardiac homogenates prepared from 8- to 9-week-old female wild-type and Atg/KO-cmAtg/TG mice (n = 6). (h) Relative luciferase activities in lysates of HepG2 cells transfected with a PPRE-luciferase reporter plasmid and a PPAR-α expression vector. The additional expression of Atgl increases luciferase activity in the absence or presence of exogenously added linoleic acid (LA). Transfection of the bacterial β-galactosidase gene (lacZ)-containing plasmid and colorimetric determination of β-galactosidase (β-gal) enzyme activity was used for normalization of transfection efficiency. Error bars show means ± s.d. *P < 0.05, **P < 0.01 and ***P < 0.001.