Is there any relationship between this incidence and methionine or other methyl donor compounds?
I think that the main reason is useing n-6 fatty acid and convert of it's to Inflammatory eicosanoids (such as PGE2, TXB2 and LTB4).
The innermost layer (tunica intima) of the aorta is made up of one layer of endothelial cells. Just like all cells, endothelial cells are are enclosed by a biological membrane consisting of a phospholipid bilayer. Per glycerophospholipid, two fatty acyl chains are esterified, which yield a roughly cylindrical molecule (the hydrocarbon region) that can easily pack in parallel to form extended sheets of membranes. A particularly central quantity is the area (A) per lipid molecule, which denotes the cross-section of the cylindrical space occupied by a phospholipid. Various studies of fully hydrated, fluid phase, model phosphatidylcholine bilayers have demonstrated that introducing one or more carbon-cabon cis double bonds into the saturated acyl chains will increase the cross-sectional area (A) by approximately 18%. Thus, an 8.5% increased interchain distance results in a 33% decreased attraction energy per pair of fatty acyl carbon atoms. Consequently, due to reduced van der Waals interactions, an increased interchain distance of a phospholipid results in more membrane flexibility.
High level of fat in diet results in an increase in plasma saturated free fatty acid levels, which cause a decrease in long-chain polyunsaturated acyl chains in membrane bilayers, decreased membrane flexibility, a decrease in all functional Class 1 glucose transporters, and ultimately, a chronic reduced ATP production, which establishes an increased endothelial dysfunction. This may be the basis of the aortic rupture.
We speculate that aerobic exercise is essential for restoring flexibility to stiff membranes. Exercise training showed direct effects on the 'browning' of white fat through irisin. The function of brown adipose tissue is to transfer energy from fatty acids into heat. Because brown adipose tissue is more saturated than white adipose tissue, and because exercise burns mostly brown fat, exercise acts to reduce the body's saturated fatty acid content, and consequently, an increase in membrane flexibility.
For more detailed information read references 1, and 2.
1. Rob N.M. Weijers. Lipid composition of cell membranes and its relevance in type 2 diabetes. Curr Diabetes Rev 2012; 8: 390-400.
2. Rob N.M. Weijers. M
thank you all another explanation is that high level of dietary fats regardless of source and type increases bile production and therefore bile acids and salts. methionine is needed to produce cysteine for taurine formation which is needed to synthesis taurocholic acid, in turn shortage of methionine will be occurred , in that case elastine synthesis will be reduced. Elastine is necessary for aortic flexibility consequently.
Supplementation of methionine more than requirement and also methyl donor like choline in high dietary fat will reduce the incidence and in agreement with Weijer,s phospholipid synthesis enhances which is effective in this regard.
With regard to medium chain saturated fatty acids, lauric and capric acid, there are published reports of antiinflammatory benefit. I suspect that this benefit derives from their amphiphilicity, membrane stabilization, increase in zeta potential (to more negative values), increase in protein-water interfacial tension, and increase in microvascular perfusion. Further, I suggest that well-controlled prospective in vivo studies, would validate my speculation. A major part of the antiinflammatory, pleiotropic properties of ascorbic acid, are likely to be based on similar considerations.
- Badges
- Science topic
- Similar topics
- Correction