Fig. 2: L-KO mice fed chow diet exhibited a distinct hepatic steatosis phenotype. | Nature Communications

Fig. 2: L-KO mice fed chow diet exhibited a distinct hepatic steatosis phenotype.

From: Deficiency of gluconeogenic enzyme PCK1 promotes metabolic-associated fatty liver disease through PI3K/AKT/PDGF axis activation in male mice

Fig. 2

a Schematic diagram of the mouse model fed the chow diet, n = 10/group. b PCK1 protein expression in WT and L-KO mouse intestine, liver, spleen, kidney, white adipose, and brown adipose confirmed by immunoblotting. The samples were derived from the same experiment and the blots were processed in parallel. This experiment was repeated for three times with similar results. c Body weight, glucose tolerance test (GTT), and insulin tolerance test (ITT) were measured in WT and L-KO mice (n = 10). d Liver weight of WT and L-KO mice (n = 10). e–g Determination of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total triglycerides (TG), total cholesterol (TC), and free fatty acid (FFA) levels in the serum or liver tissues (n = 10). h Paraffin-embedded liver sections were stained with hematoxylin and eosin (H&E), Sirius red, and F4/80. Frozen sections stained with Oil Red O. Scale bars: 50 µm. i Quantification of liver sections of WT and L-KO mice fed the chow diet (n = 10). j Levels of TNF-α and IL-6 in the liver tissues (n = 10). k Quantitative PCR analysis of liver mRNA expression (n = 10). For immunoblotting, the samples were derived from the same experiment and the blots were processed in parallel. n was the number of biologically independent mice. Data are expressed as the mean ± SEM; n.s., not significant. p values obtained via two-tailed unpaired Student’s t tests. Source data are provided as a Source Data file.

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