Warning: Undefined variable $zfal in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Deprecated: str_replace(): Passing null to parameter #3 ($subject) of type array|string is deprecated in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 530
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 531
English Wikipedia
Nephropedia Template TP (
Twit Text
DeepDyve Pubget Overpricing |
lüll Role of apoA-II in lipid metabolism and atherosclerosis: advances in the study of an enigmatic protein Blanco-Vaca F; Escola-Gil JC; Martin-Campos JM; Julve JJ Lipid Res 2001[Nov]; 42 (11): 1727-39Our understanding of apolipoprotein A-II (apoA-II) physiology is much more limited than that of apoA-I. However, important and rather surprising advances have been produced, mainly through analysis of genetically modified mice. These results reveal a positive association of apoA-II with FFA and VLDL triglyceride plasma concentrations; however, whether this is due to increased VLDL synthesis or to decreased VLDL catabolism remains a matter of controversy. As apoA-II-deficient mice present a phenotype of insulin hypersensitivity, a function of apoA-II in regulating FFA metabolism seems likely. Studies of human beings have shown the apoA-II locus to be a determinant of FFA plasma levels, and several genome-wide searches of different populations with type 2 diabetes have found linkage to an apoA-II intragenic marker, making apoA-II an attractive candidate gene for this disease. The increased concentration of apoB-containing lipoproteins present in apoA-II transgenic mice explains, in part, why these animals present increased atherosclerosis susceptibility. In addition, apoA-II transgenic mice also present impairment of two major HDL antiatherogenic functions: reverse cholesterol transport and protection of LDL oxidative modification. The apoA-II locus has also been suggested as an important genetic determinant of HDL cholesterol concentration, even though there is a major species-specific difference between the effects of mouse and human apoA-II. As antagonizing apoA-I antiatherogenic actions can hardly be considered the apoA-II function in HDL, this remains a topic for future investigations. We suggest that the existence of apoA-II or apoA-I in HDL could be an important signal for specific interaction with HDL receptors such as cubilin or heat shock protein 60.|*Lipid Metabolism[MESH]|Animals[MESH]|Apolipoprotein A-II/chemistry/deficiency/genetics/*physiology[MESH]|Apolipoproteins B/blood[MESH]|Arteriosclerosis/*genetics[MESH]|Biological Transport[MESH]|Cholesterol, HDL/blood[MESH]|Cholesterol/metabolism[MESH]|Fatty Acids, Nonesterified/blood[MESH]|Gene Expression Regulation[MESH]|Genetic Predisposition to Disease[MESH]|Humans[MESH]|Lipid Peroxidation[MESH]|Lipoproteins, VLDL/blood[MESH]|Mice[MESH]|Mice, Transgenic[MESH]|Triglycerides/blood[MESH] |