Hepatic fatty acid oxidation restrains systemic catabolism during starvation

Starvation initiates a series of metabolic adaptations to enable continuous production and delivery of nutrients to critical organs, tissues, and cells. This response is coordinated in large part by the liver that responds by liberating glucose to the circulation initially from glycogen stores followed by de novo glucose production (i.e., gluconeogenesis). Additionally, ketones are produced and provide an alternative energy source to glucose for highly oxidative tissues such as the brain. Fatty acid oxidation is critical for these processes as it provides the carbon substrate for ketogenesis (acetyl-CoA) and mitochondrial bioenergetics (ATP, NADH) to facilitate gluconeogenesis.

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