, Volume 31, Issue 3, pp 421-423
Date: 26 Mar 2010

SNP–SNP interactions within APOE gene influence plasma lipids in postmenopausal osteoporosis

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Dear Sirs,

Biological revelations have gradually started clearing the complex relationships of bones with lipids. Studies have shown that lipid profiles are related to bone mass, bone fragility and fracture risk [1, 2]. It has been observed that oxidized lipids inhibit mineralization of bone, induce osteoblastic differentiation in vascular cells, and hyperlipidemia reduces bone density in mice [3].

To understand the genetic link between lipids and osteoporosis risk, apolipoprotein E gene (APOE) is a potential candidate because of its vital contribution to both lipid and vitamin K metabolism. APOE is located on the chromosome 19q13.2 and has three codominant alleles i.e. APOE2, APOE3 and APOE4. It serves as a ligand for receptor-mediated uptake of lipoprotein particles, which are the main carriers of vitamin K, and availability of vitamin K is an essential step for the carboxylation of glutamic acid residues of osteocalcin, an important bone protein. A study has shown that decrease in bon