Beta oxidation

And so that insulin signal provides the liver with the information it needs to know to turn the volume down on some pathways and turn the volume up on other pathways.

Some other things that get turned up would be like fat synthesis, cholesterol synthesis, glycogen synthesis, the things that are getting turned down, beta oxidation, ketone body synthesis, gluconeogenesis.

These are all being turned down in that fed state, which again is being signaled by insulin.

insulin in this case in contrast the factor that opposes insulin it's like on the teeter-totter here we have insulin on one side and we have glucagon on the other side so insulin is being produced by the pancreatic beta cells glucagon is being produced by the pancreatic alpha cells so when insulin goes up glucagon goes down and as insulin goes back down glucagon begins to rise glucagon is the signal to the liver or the muscle the fat etc., that energy is in decline.

Energy availability is becoming more scarce.

What does that do? When glucagon binds to that glucagon receptor on the liver cells, it tells the liver, hey, We're kind of in a state of energetic scarcity.

That means, can you please liberate some of that stored glucose from your glycogen to help maintain blood sugar levels? Can you please turn up the knob on gluconeogenesis to make sure that we're maintaining those steady glucose levels in the bloodstream, even despite no food or carbohydrates being available? Can you turn up fatty acid beta oxidation and ketone synthesis? Because we're going to need to compensate for some of the lack of glucose and carbs coming in through the diet.

These are all intelligent responses from the liver cells to this signal of scarcity.

These are the last ones that we're going to go through, but they're really important to touch on because they fully confirm oxidative phosphorylation, ATP production at the electron transport chain from fatty acids in cancer cells.

The first one here is a twenty sixteen paper titled Enhanced OxPhos or Oxidative Phosphorylation, Glutaminolysis, and Beta-Oxidation Constitute the Metastatic Phenotype for Melanoma Cells.

And so they state here, "The four C one one positive cells also displayed an increased oxidative metabolism accompanied by enhanced rates of oxygen consumption coupled to ATP synthesis.

Furthermore, four C one one plus cells had a higher ATP content and increased succinate oxidation, which points to complex two activity and fatty acid oxidation." And the four C one one positive cells, these are metastatic cells, so the cells that are most concerning.