Fig 1: FXR deficiency increased hepatocyte lipid deposition and glucose metabolism and accelerated deterioration of hepatic steatosis in FXR-null mice. (a) A high-fat diet and FXR deficiency increased hepatocyte lipid deposition. PV: portal vein. Upper panel: bar, 200 µm, representative images H&E staining of liver tissues; middle panel: bar, 200 µm, lower panel: bar, 50 µm; both of them representative images of Oil Red O staining of liver tissues; WT: n = 3, KO: n = 3. SD: standard chow diet, HFD: high-fat diet. (b, c) FXR deficiency increased hepatic TG and FFA level, n = 10. (d) Relative mRNA levels of PDK4 and relevant glycolytic and lipogenic genes in the livers of FXR-null and WT control mice deal with the high-fat diet, HFD-WT: n = 3, HFD-KO: n = 3. (e) Detection expression of Scd1, PDK4, Srebp-1c, Acly, Acc1,CD36, Fasn, Gck, and tubulin. *P < 0.05, **P < 0.01, ****P < 0.0001.
Fig 2: Effect PDK inhibitor (dichloroacetate) on expression of enzymes involved in lipid metabolism, gluconeogenesis, and multiple hepatic signaling pathways. (a) Relative mRNA levels of PDK4 and relevant glycolytic and lipogenic genes in the livers of FXR-null, wild-type mice fed high fat diet with DCA treatment. **P < 0.01, relative to wild-type mice fed high fat diet, #P < 0.05, ##P < 0.01, ###P < 0.001, relative to FXR-null mice fed high-fat diet with DCA treatment, n = 3. (b) Representative Western blots are shown for the amounts of Fasn, Srebp-1c, Scd1, Acc1, PGC-1a, mTOR/p-mTOR, p-AMPK, p-p38, PDK4, Acly, and GCK in the livers of wild-type or FXR-null mice fed the high-fat diet with DCA treatment. Tubulin served as the loading control.
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