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Atherosclerosis is a chronic inflammatory disease driven in large part by hypercholesterolemia. It is caused by the buildup of fat, cholesterol, and other substances within the arteries and on their walls. This buildup, called plaque, can cause the arteries to narrow, obstructing blood flow and leading to other complications such as myocardial infarction or stroke.
Lipid metabolism is highly conserved between humans and zebrafish. Indeed, zebrafish express all main nuclear receptors, lipid transporters, apolipoproteins, and enzymes involved in lipoprotein metabolism. Even the activity of the cholesteryl ester transfer protein (CETP), which is naturally deficient in rodents, is detected in zebrafish plasma.
Feeding zebrafish a High Cholesterol diet (HC) results in significant hypercholesterolemia and initiation of vascular processes, which configures zebrafish as an attractive model to study mechanisms relevant to the early development of human atherosclerosis.
We offer a fast, cost-effective, and biologically relevant model for the study of cholesterol metabolism and atherosclerosis condition with a diet-induced approach.
Lipid and lipoprotein metabolism in zebrafish and humans are remarkably similar.Transparent zebrafish larvae facilitate in vivo cholesterol quantification via non-invasive confocal imaging.Vascular processes can be monitored in live animals.High throughput screening of molecules.
Lipid and lipoprotein metabolism in zebrafish and humans are remarkably similar.
Transparent zebrafish larvae facilitate in vivo cholesterol quantification via non-invasive confocal imaging.
Vascular processes can be monitored in live animals.
High throughput screening of molecules.
Early-life embryos (5th dpf) are fed a Control Diet (CD) versus a HC diet for 15 days in the presence and absence of the compound of interest. Individuals are posteriorly incubated with a fluorescent dye for the in vivo confocal visualization of cholesterol.