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Mitochondrial metabolism mediates oxidative stress and inflammation in fatty liver

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Figure

Figure 1. Propionate tracers do not perturb basal hepatic flux. Propionate (0.8 in livers perfused with gluconeogenic substrates and NEFA (effect of incomplete OAA/fumarate equilibration in the TCA cycle predicted that [U-alter ([U-model (right panel) (μmo
Figure 2. Oxidative metabolism is linked to anaplerosis and GNG in liver.
Table 1. Metabolic characteristics of 4-hour–fasted rats infused with intralipid
Figure 3. The induction of oxidative metabolism by NEFA requires increased anaplerosis/cataplerosis to cause oxidative stress and inflammation
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