Mindmap

Key ideas:

• Biological energy, i.e. ATP, and how it is produced are the basic determinants of cell function and fate.
• CII as determinant of mitochondrial phenotype.
• CII and CI are mutually inhibitory, with CII having evolved a stronger inhibitory capacity over CI as an adaptation to hypoxia.
• PUFA as a mediator of stress that becomes necessary with efficient CI-driven Q cycle is unattainable in State III respiration, involving but not limited to:
• Lipid peroxidation.
• Calcium buffering in the endoplasmic reticulum.
• Aromatase induction, producing aromatic A-ring steroids (estrogens).
• Nitric oxide synthase induction, producing the gaseous inhibitor of ETC.
• Heme oxygenase induction, inhibiting ETC through carbon monoxide and cytotoxic free iron.
• Fatty acid beta-oxidation through PPAR agonism.
• Reduced glycolytic flux through hexose pathway through PPAR agonism.
• Repression of TRE-controlled genes with co-repression of ChREBP- and SREBP-controlled genes.
• Expression of serotonergic genes involved in mammalian energy conservation through neuroendocrine stress responses.
• Biological systems on every scale have evolved nominal and back-up systems to maximise survival. Back-up systems are designed to provide survival benefits when conditions are not optimal. Disease is the result of chronic abuse of these back-up systems when nominal systems have become altogether dysfunctional.
• Fats as back-up energy substrate to glucose.
• Cortisol as back-up to thyroid hormones in maintaining energy homeostasis.
• Adrenaline as back-up to parathyroid hormone in maintaining cell responsiveness.
• Nitric oxide as back-up vasodilator to carbon dioxide.
• G6PD as back-up electron source for NADP+ to mitochondrial energy-linked transhydrogenase.