In our study the oral supplementation with BCAAem for four weeks

In our study the oral supplementation with BCAAem for four weeks was associated

with a minor change of the 2-DE pattern profile as only 10 spots out of 500 appeared differentially expressed between supplemented and unsupplemented mice. In particular the upregulated spots were identified as Apolipoprotein A-I, Complement factor B, Complement C3, Immunoglobulin light chain Wortmannin cost whereas the downregulated spots were Alpha-1-antitrypsin and an unidentified protein. Apolipoprotein A-I is a major protein component of high density lipoprotein (HDL) in the plasma and participates to the reverse cholesterol transport (RCT) from tissues to liver where it can be excreted directly into the bile or metabolized into bile salts before excretion [7, 8]. Lipid-poor Apo A-I/HDL are known to act as acceptors for

cellular lipids, and lipid efflux from cells can be mediated via cell surface proteins (ABCA1, ABCG1 and SR-BI) [9]. RCT represents the foremost mechanism underlying the anti-atherogenic effects of Apo A-I. Apart eFT-508 from its participation to the RTC HDL/Apo A-I might exert their anti-atherogenic effects through several other mechanisms. For example, it has been demonstrated that HDL/Apo A-I have anti-inflammatory activity [10] being capable to reduce oxidized lipids and its inflammatory effects [11, 12]. In experimental studies using atherosclerosis-susceptible mice (inbred C57BL/6, used in the present study), it was observed

that transgenic overexpression of human INCB28060 in vitro ApoA-I significantly protected from development of early atherosclerotic lesions [13]. Similarly, overexpression of human ApoA-I in apoE-deficient transgenic mice suppressed early atherosclerotic lesions [14]. Furthermore, knocking out apoA-I Celecoxib resulted in an accelerated atherosclerosis development in several animal models (i.e. the human apoB-transgenic female mice; the LDL receptor-deficient; the LDL receptor/apoE-deficient mice) [15, 16]. Taking into account that increasing ApoA-I production is now considered a target for coronary heart disease (CHD) risk reduction, beside pharmacological agents, several studies have focused on nutritional compounds affecting serum apoA-I concentration. For instance it has been found that, saturated fatty acids (SAFAs) and cis-monounsaturated fatty acids (cis-MUFAs), lecithin (consisting of three phospholipids; phosphatidylcholine (PC), phosphatidylethanolamine (PE), and phosphatidylinositol (PI)) and moderate amounts of ethanol [17] increase serum ApoA-I concentrations [18] but the mechanisms underlying these changes remain to be fully elucidated. Beside the energy-delivering nutrients diverse micronutrients, such as minerals (e.g. zinc, magnesium, and vanadate) and vitamins (e.g.

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