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paymanz

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And the difference is big! 100% and 50% for each ,compared to subjects with higher insulin sensitivity.

Egg yolks/milk and liver are rich source of these phospholipids. But yolks are the richest.

Skeletal muscle phosphatidylcholine and phosphatidylethanolamine are related to insulin sensitivity and respond to acute exercise in humans

Abstract
Several recent reports indicate that the balance of skeletal muscle phosphatidylcholine (PC) and phosphatidylethanolamine (PE) is a key determinant of muscle contractile function and metabolism. The purpose of this study was to determine relationships between skeletal muscle PC, PE and insulin sensitivity, and whether PC and PE are dynamically regulated in response to acute exercise in humans. Insulin sensitivity was measured via intravenous glucose tolerance in sedentary obese adults (OB; n = 14), individuals with type 2 diabetes (T2D; n = 15), and endurance-trained athletes (ATH; n = 15). Vastus lateralis muscle biopsies were obtained at rest, immediately after 90 min of cycle ergometry at 50% maximal oxygen consumption (V̇o2 max), and 2-h postexercise (recovery). Skeletal muscle PC and PE were measured via infusion-based mass spectrometry/mass spectrometry analysis. ATH had greater levels of muscle PC and PE compared with OB and T2D (P < 0.05), with total PC and PE positively relating to insulin sensitivity (both P < 0.05). Skeletal muscle PC:PE ratio was elevated in T2D compared with OB and ATH (P < 0.05), tended to be elevated in OB vs. ATH (P = 0.07), and was inversely related to insulin sensitivity among the entire cohort (r = −0.43, P = 0.01). Muscle PC and PE were altered by exercise, particularly after 2 h of recovery, in a highly group-specific manner. However, muscle PC:PE ratio remained unchanged in all groups. In summary, total muscle PC and PE are positively related to insulin sensitivity while PC:PE ratio is inversely related to insulin sensitivity in humans. A single session of exercise significantly alters skeletal muscle PC and PE levels, but not PC:PE ratio.
 
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managing

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Ok, so egg yolk good because it has both PC and PE. But you want a lower PC:PE ratio. So, what is the PC:PE ratio in eggs? Is it affected by how the hens are raised?

Are there other ways to raise PE (ie, lower the PC:PE ratio while maintaining a relatively high level of both)?
 

paymanz

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Ok, so egg yolk good because it has both PC and PE. But you want a lower PC:PE ratio. So, what is the PC:PE ratio in eggs? Is it affected by how the hens are raised?

Are there other ways to raise PE (ie, lower the PC:PE ratio while maintaining a relatively high level of both)?
Dont know,but in general these phospholipids are interesting.

MitoLipin - Dietary Supplement For Cardiolipin And Mitochondria Support

Phosphatidylethanolamine positively regulates autophagy and longevity
 

managing

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Yeah, I don't know either, lol. But I do note that @haidut product only has PC, no PE. The second link outlines the pathways of PE production:

"PE can be produced by decarboxylation of PS, as a first option at the mitochondrial membrane via phosphatidylserine decarboxylase 1 (Psd1)3, 4 or, as a second, option at the Golgi and vacuolar membranes through phosphatidylserine decarboxylase 2 (Psd2).5 As a third possibility, PE can be produced from actively retrieved extracellular ethanolamine,6, 7 which is cytidine 5'-diphosphate-activated8 and then coupled to diacylglycerol to generate PE.9 The fourth, scarcely employed PE-generating pathway is based on the lysophospholipid acylation of lyso-PE."

It seems it can be produced from phosphatidylserine, for example. @haidut would a saturated phosphatidylserine product make sense?
 

paymanz

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Ok, so egg yolk good because it has both PC and PE. But you want a lower PC:PE ratio. So, what is the PC:PE ratio in eggs? Is it affected by how the hens are raised?

Are there other ways to raise PE (ie, lower the PC:PE ratio while maintaining a relatively high level of both)?
This table shows different ratios of phospholipid in milk and yolks, also saturation index,interesting...

Health effects of dietary phospholipids

Higher PE ratio and also higher level of Sphingomyelin(SPM) are noticeable in milk.
 
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paymanz

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managing

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Good stuff. Thanks for posting. Do you know of a product that is PE only, or in a high ratio?
 

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paymanz

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This article is full of good info and references , here i excerpted some of vitamin A part of it.

Nutritional Deficiencies and Phospholipid Metabolism

Alterations in the amount of both saturated and polyunsaturated fatty acids, vitamins A, E and folate, and other micronutrients, such as zinc and magnesium, are discussed.In all cases we observe alterations in the pattern of phospholipids, the more affected ones being phosphatidylcholine, phosphatidylethanolamine and sphingomyelin.
Vitamin A:
It is well established that liver phospholipid content decreases in rats with vitamin A deficiency [50]. In contrast, it increases in guinea pig with the administration of 100,000 U.I. of vitamin A for seven days [51]. The lower content of total phospholipid in liver of vitamin A-deficient rats has been associated to a lower synthesis of phosphatidylcholine and a lower availability of fatty acids.[.......]Additionally, a significant decrease in total phospholipid content occurs in liver mitochondria of vitamin A deficient-rats giving an increased cholesterol/phospholipid relation, which suggests that membrane fluidity can be altered. This, together with the fact that mitochondrial cardiolipin content decreases, could lead to mitochondrial dysfunction.[....]Lipid metabolism is significantly modified in the heart of vitamin A-deficient rats. In the left ventricle the content of total phospholipids increases due to an increase of phosphatidylcholine, phosphatidylethanolamine and phosphatidic acid, while cardiolipin, sphingomyelin, and lisophosphatidylcholine decrease compared to the control-fed group. Vitamin A refeeding partly restores sphingomyelin and lisophosphatidylcholine contents, and completely restores cardiolipin, phosphatidylcholine, phosphatidylethanolamine and phosphatidic acid proportions to control values [.....]As it occurs in liver and heart, the increased relative percentage of phosphatidylcholine in the aorta of vitamin-A-deficient rats is explained by an increased endogenous synthesis of phosphatidylcholine and a high expression of CTP: phosphocholine cytidylyltransferase-alpha mRNA [70]. Furthermore, it has been demonstrated an increased lipoperoxidation in the aorta of vitamin-A-deficient rats [71]. The increased mass of phospholipids would be expected to be a potential source of lipid peroxides.
 
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Terma

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I like these articles but I think you can easily end up drawing wrong conclusions from this, because:
high levels of polyunsaturated fatty acids and other indices of unsaturation in skeletal muscle phospholipids are positively associated with estimates (e.g., fasting plasma insulin) and direct measures (e.g., hyperinsulinemic-euglycemic clamp) of insulin sensitivity
...
Furthermore, our finding that low levels of polyunsaturation and long-chain acyl groups in muscle phospholipids are associated with insulin resistance is in agreement with previous reports

I'd wager "insulin sensitivity" in skeletal muscle after acute exercise is not the best marker of health?

The PC:PE ratio is also affected by the PEMT enzyme in liver which converts PE to PC: Phosphatidylethanolamine N-methyltransferase - Wikipedia
This complicates things, because although dietary choline can be incorporate through the Kennedy pathway (most of it IIRC), part of it also fuels methylation which then fuels PEMT. (most likely betaine fuels PEMT the most, but didn't confirm this)

I haven't read every paragraph, but on the surface I'm not sure any of these mention the saturation of PC itself.

One thing that determines the saturation of PC is whether it's synthesized through PEMT or through the Kennedy pathway (influenced by uridine too): Molecular distinction of phosphatidylcholine synthesis between the CDP-choline pathway and phosphatidylethanolamine methylation pathway. - PubMed - NCBI
In the PEMT-expressing RH7777 cells, comparison between
PC species newly synthesized from the CDP-choline pathway
(Fig. 2D) and that from the PE methylation (Fig. 2F) revealed
a clear distinction. The major species of the PC derived from
the CDP-choline pathway were diacyl 16:0/18:1, 18:0/18:2, and
18:1/18:1, which together made up a majority of the choline-
derived PC. On the other hand, PC derived from the methyla-
tion pathway contained significantly more long chain, polyun-
saturated PC species (18:1/18:1; 18:0/18:2; 18:2/20:4; 18:1/20:4;
18:0/20:4; 18:0/22:6; 18:1/22:5). These findings were in agree-
ment in principal with the previous report that purified PEMT
prefers the long chain polyunsaturated PE as substrate (26) for
PC synthesis.

Even more generally, PE is more likely to be unsaturated than PC (see studies on brain phospholipid composition e.g. https://sci-hub.la/http://onlinelib...ionid=A53F43379A3C7FAD17CC8E0C24104519.f03t01).

Moreover this is dependent on how much of this exported from the liver is getting incorporated into skeletal muscle. I'll stop here because you can see this gets convoluted to draw dietary conclusions from without specific in vivo experiments. A lot of studies are read are from ~1999, so maybe you can find newer ones.
 

Terma

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By the way, milk contains some UMP and orotic acid (uridine precursor) which probably contribute to the Kennedy pathway somewhat. I don't think those other foods do but didn't double check.
 

paymanz

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I like these articles but I think you can easily end up drawing wrong conclusions from this, because:


I'd wager "insulin sensitivity" in skeletal muscle after acute exercise is not the best marker of health?

The PC:PE ratio is also affected by the PEMT enzyme in liver which converts PE to PC: Phosphatidylethanolamine N-methyltransferase - Wikipedia
This complicates things, because although dietary choline can be incorporate through the Kennedy pathway (most of it IIRC), part of it also fuels methylation which then fuels PEMT. (most likely betaine fuels PEMT the most, but didn't confirm this)

I haven't read every paragraph, but on the surface I'm not sure any of these mention the saturation of PC itself.

One thing that determines the saturation of PC is whether it's synthesized through PEMT or through the Kennedy pathway (influenced by uridine too): Molecular distinction of phosphatidylcholine synthesis between the CDP-choline pathway and phosphatidylethanolamine methylation pathway. - PubMed - NCBI


Even more generally, PE is more likely to be unsaturated than PC (see studies on brain phospholipid composition e.g. https://sci-hub.la/http://onlinelib...ionid=A53F43379A3C7FAD17CC8E0C24104519.f03t01).

Moreover this is dependent on how much of this exported from the liver is getting incorporated into skeletal muscle. I'll stop here because you can see this gets convoluted to draw dietary conclusions from without specific in vivo experiments. A lot of studies are read are from ~1999, so maybe you can find newer ones.
Thanks ,i havent researched on this stuff that much, but the links i shared from haidut's mitolipin thread and other links i shared(the egg consumption and insulin sensitivity ,for example) many of them shows some dietary phospholipids and choline may be protective and beneficial. Regardless of the ratio.

Yes ,these are complicated and thinking about manipulating their ratio makes it more even complicated.
 

paymanz

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One thing that determines the saturation of PC is whether it's synthesized through PEMT or through the Kennedy pathway (influenced by
Idk about that pathway but also the availability of pufa/mufa/sfa fatty acids affets the saturation of phospholipids that synthesized in body.

And regarding dietary PLs saturation, milk's are really good ,while egg has some pufa,it still is not that bad ,it has decent saturated and monosaturated ones too.more than pufa.

I agree ,all of these articles speak about benefits of unsaturated phospholipids to be superior,but i stick with peats view.

I just found very few ones reporting better insulin sensitivity with more saturation of PLs.
 

Terma

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Idk about that pathway but also the availability of pufa/mufa/sfa fatty acids affets the saturation of phospholipids that synthesized in body.

And regarding dietary PLs saturation, milk's are really good ,while egg has some pufa,it still is not that bad ,it has decent saturated and monosaturated ones too.more than pufa.

I agree ,all of these articles speak about benefits of unsaturated phospholipids to be superior,but i stick with peats view.

I just found very few ones reporting better insulin sensitivity with more saturation of PLs.

I agree dairy is most likely the best of all the foods mentioned for this, even if it's not that high in choline and I can't have much of it anymore. Haidut's supplement could be even better (depending how much gets absorbed intact, didn't read) but it seems underdosed to me.
 

Terma

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Ok this is good, this link you posted earlier confirms my suspicion in parenthesis above:
Pemt−/− Mice Are Resistant to Diet-induced Obesity When Supplemented with Betaine
To examine the mechanism by which choline modulates the development of obesity, we fed Pemt+/+ and Pemt−/− mice the HF diet (1.3 g of choline/kg of diet) supplemented with betaine (2.7 g/kg of diet). Betaine is an important methyl-group donor and osmolyte (35, 36). In hepatocytes, ∼60% of choline is converted to betaine (37). Oral supplementation of betaine has been shown to alleviate both alcoholic- and non-alcoholic fatty liver disease (38, 39), prevent sucrose-induced steatosis (40), and reduce atherosclerosis in methyl group-deficient animals (41). We, therefore, tested the idea that the effects of choline supplementation in Pemt−/− mice fed the HF diet were due to increased supply of betaine, rather than choline, supply. Pemt+/+ and Pemt−/− mice gained approximately the same amount of weight when fed the HFCS diet for 10 weeks (Fig. 7A). However, the Pemt+/+ mice fed the betaine-supplemented diet gained weight, whereas the Pemt−/− mice did not (Fig. 8A). In addition, the difference in glucose tolerance and insulin resistance observed between Pemt+/+ and Pemt−/− mice fed the HF diet (Fig. 2, G and F) was prevented by choline (Fig. 7, B and C) but not by betaine (Fig. 8, B and C).

So betaine stimulates almost exclusively PEMT through methylation, while 60% of choline (experimental mouse figure, this will be different in vivo in humans) should go to PEMT.

(I didn't remember if there was a significant pathway through which betaine could convert back to choline or significantly spare existing choline - though still possible this latter case applies in a less experimental scenario)

So if you combine this with the information I posted above, taking TMG or other sources of betaine should produce more unsaturated phospholipids than taking choline and uridine (or CDP-choline, same thing).

[or, if you prefer, methylation in general should produce more unsaturated, so getting less methionine and more choline might be preferable]
 
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