Figure 1.

Suggested liver metastatic cancer metabolism in normal diet or fasting-mimicking diet. In the presence of glucose, the breast cancer cells metastasized to the liver mainly go through glycolysis to produce pyruvate, which is converted to acetyl-CoA via oxidative decarboxylation. Acetyl-CoA enters the tricarboxylic acid cycle (TCA cycle) and generates adenosine-3-phosphate (ATP) for cell survival and proliferation. Excessive glucose can be stored as glycogen for further usage. When glucose is limited (under a fasting-mimicking diet), the cancer cells switch to acquire ATP by fatty acid oxidation. The fatty acid oxidation is also highly activated in peripheral hepatocytes, where abundant acetyl-CoA feeds into ketogenesis and produces a large amount of acetoacetate and β-hydroxybutyrate. The liver does not use ketone bodies for energy because it lacks the necessary enzyme thiophorase (beta ketoacyl-CoA transferase). The unclear part is how these released ketone bodies function on breast cancer cells.