Impaired IIS causes a reduction of intracellular glucose availability which then induces mitochondrial metabolism of alternate energy substrates, i.e., fatty acids and/or amino acids, culminating in transiently increased ROS levels
- Glycolysis increases cytoplasmic ROS levels (in the form of the aldehyde intermediates). wonder how this competes with mitohormesis. also i wonder if mitohormesis could explain why some benefit from keto diets (though meat-heavy keto diets aren't very healthy for other reasons)
- Also isn't krebs cycle (happens wth the acetyl-coa leftovers in mitochondria also the primary source of energy after glycolysis? is it possible that beta-oxidation and proline catabolism might generate a few more free radi...