Skip to main content
. 2019 Jul 12;27(10):1848–1862. doi: 10.1016/j.ymthe.2019.06.017

Figure 3.

Figure 3

R-Tf-D-LP4 Peptide Treatment of HFD-32-Fed Mice Altered Liver Lipid Metabolism and Steatosis Pathology

(A) Immunoblots of several proteins in livers from ND-fed; HFD-32-fed; and HFD-32-fed, peptide-treated mice. (B) IHC of CPT1 with the relative intensity (n = 3 liver sections) is presented in parentheses. (C) Immunoblot quantitative analysis. (D) qRT-PCR analyses of mRNA of proteins associated with lipid metabolism in livers from ND-fed (black bars); HFD-32-fed (dark gray bars); and HFD-32-fed, peptide-treated (light gray bars) mice. Transcription factors and co-activators involved in lipid metabolism regulation (E) and mRNA levels of UCP1 and UCP2, associated with thermogenic respiration (F), were analyzed in the same groups of mice as above. (G) qRT-PCR analysis of mRNA levels of proteins associated with lipid biosynthesis in livers from ND-fed (black bars); HFD-32-fed (dark gray bars); and HFD-32-fed, peptide-treated (light gray bars) mice. Results are means ± SEM (n = 3–5; *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001). Immunoblot (H) and quantitative analysis (I) of ACC1 and FAS. β-actin served as the loading control.