CD36 is a class B scavenger receptor that is involved in fatty acid and glucose metabolism, heart disease, gustatory taste of lipid/fat, and lipid metabolism.  CD36 also functions as a microglial surface receptor for amyloid beta peptide.  These mutant mice carry a targeted mutation in which exon 3, which encodes the first 40 amino acids and the translation initiation site, is replaced by a NEO cassette (in opposite orientation).  Mice that are homozygous for the targeted mutation are viable and fertile, but smaller in size than controls.  No gene product (protein) is detected by immunoprecipitation or Western blot analysis of fat, muscle, heart, macrophages, liver, and endothelial cells from homozygotes.  Homozygotes eat less and have a reduced preference for food rich in fat. Mutant homozygous mice exhibit increased plasma ketone (beta hydroxybutyrate) and circulating HDL cholesterol levels; elevated fasting levels of nonesterified free fatty acids, and triacylglycerol; and decreased fasting blood glucose levels, when compared to controls.  Uptake of fatty acids is decreased in muscle, heart and adipose tissue in homozygotes.  IgM levels and transitional B cells in spleen and bone are increased in  homozygotes.  The increase in cerebral blood flow induced by amyloid-beta peptide is absent in homozygotes.  Following experimentally induced injury, regenerating nerves have thinner myelination and more macrophages present than seen in controls.  The resting coronary resistance blood pressure is lower in homozygotes than in controls.

In this Cd36 knockout strain, a range of lipid-related metabolic traits are observed: reduced preference for food rich in fat, altered fatty acid uptake and lowered food intake. They may be useful in studies of taste preference, glucose metabolism, lipid homeostasis, hemostasis, thrombosis, malaria, inflammation, and atherogenesis. &nbsp;

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