Figure 2. TGH deficiency ameliorates steatosis through various metabolic pathways.

(a) Perilipin 2 abundance evaluated by immunoblot in HFD fed WT and Tgh^−/− mice, Immunoblotting for PDI was used as control for protein loading. (b) mRNA expression of Cidea in HFD fed WT and Tgh^−/− mice (n = 5). (c) De novo lipogenesis was assessed by synthesis of FA from [³H]acetic acid that are incorporated into TG in primary hepatocytes isolated from chow and HFD fed WT and Tgh^−/− mice. (d) mRNA expression of Srebf1c. (e) Liver SCD-1 abundance in HFD fed WT and Tgh^−/− mice was assessed by immunoblotting. Calnexin immunoblotting was used as control for protein loading. (f) Immunoblotting for liver phospho-(Ser79) acetyl-CoA carboxylase (ACC) and total ACC in HFD fed WT and Tgh^−/− mice. Immunoreactive bands were quantified by the densitometric analysis and the p-ACC/ACC ratio was calculated. (g) mRNA expression of genes related to FA oxidation (n = 5,6). (h) Hepatic In vivo insulin signaling. Immunoreactive bands were quantified by the densitometric analysis and the pAkt/total-Akt ratio was calculated in each condition. Data are mean ± SEM, *P < 0.05, **P < 0.01, ***P < 0.001 vs WT group on the same diet condition, ^#P < 0.05, ^##P < 0.01, ^###P < 0.001 vs chow diet fed group in the same genotype.