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Journal of Lipid Research, Vol. 42, 1727-1739, November 2001
Copyright © 2001 by Lipid Research, Inc.

Review Article

Role of apoA-II in lipid metabolism and atherosclerosis: advances in the study of an enigmatic protein

Correspondence to: Francisco Blanco-Vaca, To whom correspondence should be addressed., fblancova{at}hsp.santpau.es (E-mail)

Our 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. — Blanco-Vaca, F., J. C. Escolà-Gil, J. M. Martín-Campos, and J. Julve. Role of apoA-II in lipid metabolism and atherosclerosis: advances in the study of an enigmatic protein. J. Lipid Res. 2001. 42: 1727–1739.

Supplementary key words: apoA-I, apoB, HDL, hyperlipidemia, hypertriglyceridemia, insulin resistance, triglycerides, type 2 diabetes, VLDL

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