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- W2089632170 abstract "Cholesterol's (CH) function cannot be to stiffen membranes because: 1) We synthesize CH but cannot burn it for energy; 2) Mankind has over 100 genes devoted to CH management, regulation, trucking, biosynthesis, degradation, etc. 3) Unlike CH plant sterols have branches on their sidechains. 4) Most cultured animal cells die without CH. 5) We have >2 ABC intestinal transporters that selectively block phytosterol uptake. 6) The lipid mole fraction of CH rises and falls with the [Na+] that faces the membrane. Literature evidence is here gathered that shows cells in vivo leak Na+ due to the ΔΨ and the blood [Na+] which is 0.1M. Although the Na+ leakage is slow (10−12 cm/sec) compared to H+ leakage (10−5 cm/sec), the high [Na+] makes them equivalent. Furthermore the presence of 1/3 mole% CH, as typically found in membranes facing blood, reduces the Na+ leakage to 1/3 that found in bilayers lacking CH. FDA data suggest excess statins taken by ∼200 patients in the last 8 years resulted in lethal rhabdomyolysis (RH). If cholesterol's function is to limit Na+ leakage (Prog. Lipid Res. 40 (2001) 299), then 3 times as much ATP is needed to compensate for leaked Na+. Muscle cells, lacking a pentose shunt cannot make much NADPH, which is essential for CH synthesis. Such a CH deficiency in muscle would provoke Na+ leakage into cells that may burst because of osmotic swelling. A common feature of RH in autopsies is that salt is found in the muscle cells. Due to the branches on their side chains, plant sterols appear to be designed to inhibit H+ leakage (op cit.). They are only found where the plasma membrane has a H+ gradient. CH is only found in cells where the plasma membranes facing Na+." @default.
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- W2089632170 date "2010-01-01" @default.
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- W2089632170 title "Cholesterol Deficiency, Statins and Rhabdomyolysis" @default.
- W2089632170 doi "https://doi.org/10.1016/j.bpj.2009.12.1780" @default.
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