@alfredoolivas said in PC choline to stabilize membranes:
Your body will break down the PC into lysophosphatidylcholine + free fatty acids.
Back in the body, your body will a join the lysophosphatidylcholine with circulating fatty acids. When the enter the cell, it breakds down back into lysophosphatidylcholine, and rejoins with fatty acids in the cell back into PC.So as long, as you eat saturated fat with the PC, then basically, you will be receiving saturated PC.
This doesn't seem to make enough sense for me. The fact there is a kind of lipolysis makes the fact even more crucial that there be a saturated PC. If the original PC contains PUFAs like linoleic acid (18:2), those PUFAs are released into circulation and can be incorporated into tissues, including mitochondrial and cellular membranes, where they increase oxidative stress and inflammation.
Even if lysoPC is re-acylated with saturated fats, some PUFA has already entered the system, and it’s not excreted immediately. Crucially, the enzyme LPCAT3 responsible for re-acylation, strongly prefers polyunsaturated fatty acyl-CoAs, especially arachidonic acid. Although, I tend to use different language in describing that, as more or less a hijacking than anything else.
This means that even in a high-saturated-fat context, the body prioritizes incorporating PUFAs into PC when available. And although metabolcally and typically, saturated fats are preferential fuel over PUFA, in the case of the building PC, PUFA wins, hence why I prefer the term hijack. So if dietary PC contains PUFAs, they’re more likely to be retained and recycled, not replaced.
Studies show that LPCAT3 knockout mice have reduced PUFA content in PC and are protected from diet-induced fatty liver! This was a indirect evidence incidentally, because the researchers were looking at total overall PC from high fat diet as related to disease progression. But guess what, the high fat diet is your typical formula: 25 grams Soybean Oil and almost 300 grams pig lard. This confirming that this enzyme drives PUFA incorporation into membranes. The takeaway being it is doubly important we use saturated PC.
High-fat diet-induced upregulation of exosomal phosphatidylcholine contributes to insulin resistance
Anil Kumar, et al
