| First Author | Millar JS | Year | 2002 |
| Journal | Arterioscler Thromb Vasc Biol | Volume | 22 |
| Issue | 6 | Pages | 989-94 |
| PubMed ID | 12067909 | Mgi Jnum | J:103299 |
| Mgi Id | MGI:3609098 | Doi | 10.1161/01.atv.0000018304.30943.06 |
| Citation | Millar JS, et al. (2002) Normal production rate of apolipoprotein B in LDL receptor-deficient mice. Arterioscler Thromb Vasc Biol 22(6):989-94 |
| abstractText | The low density lipoprotein (LDL) receptor is well known for its role in mediating the removal of apolipoprotein B (apoB)-containing lipoproteins from plasma. Results from in vitro studies in primary mouse hepatocytes suggest that the LDL receptor may also have a role in the regulation of very low density lipoprotein (VLDL) production. We conducted in vivo experiments using LDLR-/-, LDLR+/-, and wild-type mice (LDLR indicates LDL receptor gene) in which the production rate of VLDL was measured after the injection of [35S]methionine and the lipase inhibitor Triton WR1339. Despite the fact that LDLR-/- mice had a 3.7-fold higher total cholesterol level and a 2.1-fold higher triglyceride level than those of the wild-type mice, there was no difference in the production rate of VLDL triglyceride or VLDL apoB between these groups of animals. Experiments were also conducted in apobec1-/- mice, which make only apoB-100, the form of apoB that binds to the LDL receptor. Interestingly, the apobec1-/- mice had a significantly higher production rate of apoB than did the wild-type mice. However, despite significant differences in total cholesterol and triglyceride levels, there was no difference in the production rate of total or VLDL triglyceride or VLDL apoB between LDLR-/- and LDLR+/- mice on an apobec1-/- background. These results indicate that the LDL receptor has no effect on the production rate of VLDL triglyceride or apoB in vivo in mice. |
