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As we all know, PUFAs are a metabolic toxin. One of the mechanisms how a high fat diet promotes obesity and metabolic syndrome is by remodeling cardiolipin. Cardiolipin is a unique mitochondrial phospholipid that contains 4 fatty acids. Its main goal is to stabilize the complexes of the electron transport chain so that energy production can be optimized. Peat has mentioned that babies are born with their cardiolipin completely saturated (consisting of saturated fat). As they start to eat more PUFAs, their cardiolipin becomes more unsaturated (first linoleic acid, then more unsaturated fat such as arachidonic acid, EPA and DHA), which makes it prone to oxidation by free radicals. Also, PUFAs are fluid, which reduces the stability of the complexes of the ETC, thus reducing energy production. And this is exactly what this study found.
"Compared to the control diet, the high fat diet remodeled liver mitochondrial phospholipid acyl chain composition by 0.6-5.3-fold with notable increases in n-6 and n-3 polyunsaturation. The remodeling in the liver was accompanied by diminished complex I to III respiratory enzyme activity by 3.5-fold. Finally, qRT-PCR analyses demonstrated an upregulation of liver mRNA levels of tafazzin, which contributes to cardiolipin remodeling. Altogether, these results demonstrate that diet-induced obesity remodels acyl chains in the mitochondrial phospholipidome and exerts tissue specific impairments of respiratory enzyme activity." (R)
So all in all, even without being damaged by oxidative stress, both omega 6 and 3 can unsaturate cardiolipin and make the ETC less effective. Once the ETC becomes less effective, there will be more electron leak, which will damage the unsaturated cardiolipin and serious cell damage and possible cell death as well.
Depleting PUFA is one of the best ways to undo this. Feeding rats saturated fat restore cardiolipin back to normal and rescued defective energy metabolism.
"Compared to the control diet, the high fat diet remodeled liver mitochondrial phospholipid acyl chain composition by 0.6-5.3-fold with notable increases in n-6 and n-3 polyunsaturation. The remodeling in the liver was accompanied by diminished complex I to III respiratory enzyme activity by 3.5-fold. Finally, qRT-PCR analyses demonstrated an upregulation of liver mRNA levels of tafazzin, which contributes to cardiolipin remodeling. Altogether, these results demonstrate that diet-induced obesity remodels acyl chains in the mitochondrial phospholipidome and exerts tissue specific impairments of respiratory enzyme activity." (R)
So all in all, even without being damaged by oxidative stress, both omega 6 and 3 can unsaturate cardiolipin and make the ETC less effective. Once the ETC becomes less effective, there will be more electron leak, which will damage the unsaturated cardiolipin and serious cell damage and possible cell death as well.
Depleting PUFA is one of the best ways to undo this. Feeding rats saturated fat restore cardiolipin back to normal and rescued defective energy metabolism.