Figure 6.

A, liver DC-CoA content was increased by CFB treatment in the fasting rats, as reduced by 4-MP.B, liver peroxisomal β-oxidation activity was enhanced by the treatment with CFB and inhibited by TDYA. C, CFB treatment increased succinate generation in the liver of the fasting rats, as reduced by 4-MP or TDYA. D, CFB robustly elevated plasma βOHB/AcAc ratio in the fasting rats, as reduced by 4-MP or TDYA. E and F, CFB treatment resulted in hepatic accumulation of 3-OH-CoA (E) and 2-enoyl-CoA (F) intermediates in the fasting rats, as reduced by treatment with 4-MP or TDYA. G, TDYA or 4-MP treatment stimulated ketone body formation in the fasting rats, while CFB decreased plasma ketone body. H, liver LC-acyl-CoA was significantly higher in CFB treated rats and reduced by the treatment with 4-MP or TDYA. I, CFB treatment led to hepatic TAG accumulation in the fasting rats, as reduced by 4-MP or TDYA. J, Effects of CFB, 4-MP or TDYA upon hepatic steatosis in the fasting rats. Magnification: 200×. Scale bar = 20 μm. K, CFB treatment increased VLDL-TAG secretion rate in the fasting rats, as reduced by the treatment with 4-MP or TDYA. L, CFB treatment increased plasma TAG level in the fasting rats, as reduced by 4-MP or TDYA. M, CFB treatment increased hydrogen peroxide generation in the liver of the fasting rat, as reduced by 4-MP or TDYA. N, liver TBARS content increased significantly by CFB and reduced by the treatment with 4-MP or TDYA. Mean ± SEM, n = 8, ∗p < 0.05 by t-test between paired conditions.