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. 2019 Dec 3;318(2):E145–E151. doi: 10.1152/ajpendo.00370.2019

Fig. 1.

Fig. 1.

Validation of mouse model. dTG, mice with combined and tamoxifen-inducible skeletal muscle-specific overexpression of sirtuin 1 (SIRT1) and knockout of general control of amino acid synthesis 5 (GCN5). A: transcript levels of Sirt1 and Gcn5 normalized to Tbp in wild-type (WT) and dTG skeletal muscle (n = 7/genotype). Representative blot (B) and quantification (C) of protein abundance of SIRT1 and GCN5 in skeletal muscle from WT and dTG mice. Bar graphs show protein abundance in skeletal muscle relative to GAPDH (n = 6/genotype). D: transcript levels of Pgc-1α, and its target genes Acadl, Acadvl, Cox5b, Cs, Cycs, Sdhb, and Sirt3 normalized to PolR2A in WT and dTG skeletal muscle (n = 7/genotype). Representative images (E) and quantification (F) of protein abundance of PGC-1α targets ACADVL, ACADL, and SIRT3 in skeletal muscle from WT and dTG mice. Bar graphs show protein abundance in skeletal muscle relative to Ponceau S (n = 6/genotype). G: transcript levels of Hdac2, Hdac3, Sirt2, Hat1, Ep300, and Kat2b normalized to Tbp in WT and dTG skeletal muscle (n = 7/genotype). H: body weight, lean muscle mass, and fat mass from dTG and WT mice (WT n = 4, dTG n = 7). I: fat mass expressed as percent body weight (WT n = 4, dTG n = 7). Data are reported as means ± SE. *P < 0.05 vs. WT (A–I: unpaired Student’s t test. PGC-1α, peroxisome proliferator-activated receptor-γ coactivator-α; ACADL, acyl-CoA dehydrogenase long chain; ACADVL, acyl-CoA dehydrogenase very long chain.