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. Author manuscript; available in PMC: 2011 Aug 1.
Published in final edited form as: Biochim Biophys Acta. 2009 Dec 11;1804(8):1676–1683. doi: 10.1016/j.bbapap.2009.11.023

Figure 2.

Figure 2

Conditions that increase PGC-1α activity, such as fasting, increase the oxidation of fatty acids and decrease the oxidation of glucose in skeletal muscle. Genes that are upregulated by increases in PGC-1α activity are indicated in green whereas those that are downregulated are indicated in red and are underlined. PGC-1α increases the rates at which both glucose and fatty acids are transported into myocytes. Both the rate of glycolysis and the rate at which glucose-derived pyruvate is converted into acetyl-CoA, however, are significantly reduced by PGC-1α. Fatty acid transport into mitochondria is significantly enhanced, on the other hand, by PGC-1α. The rate at which fatty acids are oxidized in the mitochondrion is similarly increased, resulting in an increase in the acetyl-CoA pool derived from this macronutrient. Genes involved in TCA cycle flux, electron transport, and proton-coupled ATP synthesis are upregulated by PGC-1α, improving the efficiency with which ATP can be generated from fatty acids.