Transcript analysis of infected and control high-fat diet fed ApoE<sup>-/-</sup> mice confirm that <i>ApoC1, Psat1</i>, and <i>Gys1</i> are all altered by infection, suggesting that altered hepatic macrophage metabolism is associated with <i>S. mansoni</i>- induced protection from hyperlipidemia, atherosclerosis, and glucose intolerance.
Cross-breeding of APOC1 mice on an apoE-deficient background resulted in a marked 55-fold increase in TG, confirming that the apoC-I-induced hyperlipidemiacannot merely be attributed to blockade of apoE-recognizing hepatic lipoprotein receptors.
Previous studies have shown that APOC1 transgenic mice develop hyperlipidaemia primarily because of an impaired hepatic uptake of very low density lipoprotein (VLDL).
Remarkably, Ad-VLDLR treatment did not reduce hyperlipidaemia in transgenic mice overexpressing human APOC1, irrespective of both the level of transgenic expression and the presence of the LDLR, whereas Ad-VLDLR treatment did reverse hyperlipidaemia in LDLR-/- and wild-type mice.