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. Author manuscript; available in PMC: 2010 Jun 2.
Published in final edited form as: Circulation. 2009 May 18;119(21):2818–2828. doi: 10.1161/CIRCULATIONAHA.108.832915

Figure 4.

Figure 4

Mechanisms by which high intracellular glucose remodel metabolic network to perpetuate glucose oxidation and to resist the stimulation of fatty acids during high fat diet feeding. Increased intracellular glucose downregulates the expression of 3-oxoacid CoA transferase (SCOT), a key enzyme in ketone metabolism, resulting in decreased oxidation of ketones. High glucose also downregulates PPARα expression, which limits the stimulatory effects of fatty acids on the expression of array of genes involved in fatty acid uptake and fatty acid oxidation (FAO) such as CD36 and CPT-1. Independent of PPARα mechanisms, glucose induced expression of acetyl-CoA carboxylase (ACC) that leads to increased synthesis of malonyl-CoA which inhibits fatty acid entering mitochondria via CPT-1 and promotes lipid synthesis and storage in the cytosol.