The mice are hemizygous for the human apolipoprotein A2 (ApoA2) gene expressed under the control of the homologous promoter (-911/+2045). They are humanized because they are deficient in mouse ApoAII following backcrosses with APOA2 Knockout mice (KO-ApoA2 described in ref. 1). KO-ApoA2 mice have been fully backcrossed into the C57BL/6 background before mating with human ApoAII transgenic mice.
ApoAII is expressed only in liver. Its plasma concentration is 50 mg/dl with chow diet (1.5 to 2 times the physiological concentration in humans), and increases up to 70 mg/dl with a high fat diet.
In the fed state, plasma HDL levels are decreased by 45% (compared to C57BL/6 mice) and triglycerides are increased up to 10-fold, due to decreased VLDL catabolism. In the fasted state, mice display a 34% reduction in HDL and normal triglyceridemia (2).