Mouse Genome Informatics
hm1
    Apoetm1(APOE*2)Mae/Apoetm1(APOE*2)Mae
involves: 129P2/OlaHsd * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
cardiovascular system
• all spontaneously develop atherosclerotic plaques in the proximal aorta, even on a regular diet
• an atherogenic diet, high in fat and cholesterol, exacerbates development of atherosclerosis

homeostasis/metabolism
• delay in clearance of beta-migrating VLDL particles (J:48565)
• accumulation of beta-VLDL particles in plasma; more than 65% of the total cholesterol is in the VLDL-intermediate density lipoprotein range (J:48565)
• beta-VLDL particles are highly enriched in cholesterol ester and have a VLDL cholesterol-to-triglyceride ratio of 0.76 compared with 0.03 in Apoetm2(APOE)Mae homozygotes (J:48565)
• unable to clear VLDL from plasma completely 4 hours post-injection (J:67282)
• develop type III hyperlipoproteinemia, even on a low low-fat and low-cholesterol diet (J:48565)
• plasma cholesterol levels are 2-3 times those of controls, however HDL cholesterol levels are no different from controls (J:48565)
• plasma triglyceride levels are 2-3 times those of controls (J:48565)
• develop hyperlipidemia, even on a low-fat and low-cholesterol diet
• an atherogenic diet, high in fat and cholesterol, exacerbates the hyperlipidemia
• an atherogenic diet, high in fat and cholesterol, exacerbates development of xanthomas; the atherogenic diet causes swelling of the carpi, paws, and periorbital area and a dramatic deposition of lipid under the skin

liver/biliary system
N
• livers of mutants on the atherogenic diet appear normal compared to wild-type which are enlarged and pale, indicating protection of hepatocytes from fatty changes (J:48565)

pigmentation
• aged (65-127 weeks) mutants fed a high-fat diet exhibit retinal pigment epithelium (RPE) changes such as RPE vacuolization, RPE mottling, including hyperpigmentation and hypopigmentation and Bruch's membrane thickening
• aged mutants fed a high-fat diet exhibit accumulation of deposits between the RPE and Bruch's membrane of varying thickness and RPE basal infoldings that are disorganized or absent

vision/eye
• aged (65-127 weeks) mutants fed a high-fat diet exhibit retinal pigment epithelium (RPE) changes such as RPE vacuolization, RPE mottling, including hyperpigmentation and hypopigmentation and Bruch's membrane thickening
• aged mutants fed a high-fat diet exhibit accumulation of deposits between the RPE and Bruch's membrane of varying thickness and RPE basal infoldings that are disorganized or absent
• thickening of Bruch's membrane

Mouse Models of Human Disease
OMIM IDRef(s)
Apolipoprotein E; APOE 107741 J:48565


Mouse Genome Informatics
cx2
    Apoetm1(APOE*2)Mae/Apoetm1(APOE*2)Mae
Ldlrtm1(LDLR)Mae/Ldlr+

involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
homeostasis/metabolism
• exhibit increased clearance of non-HDL lipoproteins (VLDL and LDL) from plasma
• do not develop type III hyperlipoproteinemia, exhibiting normal plasma cholesterol and triglyceride levels on a normal chow diet
• more resistant to diet-induced hyperlipidemia than single Apoetm1(APOE)Mae homozygotes


Mouse Genome Informatics
cx3
    Apobec1tm1Rub/Apobec1tm1Rub
Apoetm1(APOE*2)Mae/Apoetm1(APOE*2)Mae

involves: 129P2/OlaHsd * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
homeostasis/metabolism
• 60% in males compared to in Apoetm1(APOE*2)Mae homozygotes
• 18% in female mice compared to in Apoetm1(APOE*2)Mae homozygotes
• in male and female mice compared to in Apoetm1(APOE*2)Mae homozygotes
• female and male mice exhibit increased serum triglyceride levels (60% and 100%) compared to in Apoetm1(APOE*2)Mae homozygotes
• compared to in Apoetm1(APOE*2)Mae homozygotes