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==Type III Hyperlipoproteinemia== | ==Type III Hyperlipoproteinemia== | ||
Familial Type III hyperlipoproteinemia is a genetic lipid disorder that is marked by an increase in the concentrations of plasma cholesterol and triglyceride levels '<ref>Rall, Stanley C. et al. 1981. Human apolipoprotein e the complete amino acid sequence. The Journal of Biological Chemistry 257(8):4171-4178.</ref>'. Normally, in individuals whose apoE is functional, chylomicron remnants and VLDL remnants are rapidly removed from circulation via receptor-mediated endocytosis within the liver. However, this condition develops as a result of apoE that has impaired clearance abilities. When a defect in apoE of this nature is present, delayed clearance in the plasma of triglyceride-rich lipoprotein remants results; significantly elevated levels of cholesterol-encriched remnant lipoproteins are a defining feature of this disorder '<ref>OMIM.Omim.org/entry/107741.</ref>' '<ref>Kashyap, VS et al. 1995. Apolipoprotein E Deficiency in Mice: Gene Replacement and | Familial Type III hyperlipoproteinemia is a genetic lipid disorder that is marked by an increase in the concentrations of plasma cholesterol and triglyceride levels '<ref>Rall, Stanley C. et al. 1981. Human apolipoprotein e the complete amino acid sequence. The Journal of Biological Chemistry 257(8):4171-4178.</ref>'. Normally, in individuals whose apoE is functional, chylomicron remnants and VLDL remnants are rapidly removed from circulation via receptor-mediated endocytosis within the liver. However, this condition develops as a result of apoE that has impaired clearance abilities. When a defect in apoE of this nature is present, delayed clearance in the plasma of triglyceride-rich lipoprotein remants results; significantly elevated levels of cholesterol-encriched remnant lipoproteins are a defining feature of this disorder '<ref>OMIM.Omim.org/entry/107741.</ref>' '<ref>Kashyap, VS et al. 1995. Apolipoprotein E Deficiency in Mice: Gene Replacement and | ||
Prevention of Atherosclerosis Using Adenovirus Vectors. The Journal of Clinical Investigation 96:1612-1620.</ref>'. Individuals homozygous for the ε2 allele are most susceptible. The E2 isoform of apoE exhibits weak or defective binding of remnants to hepatic lipoprotein receptors; the E2 isoform also clears these remnants from the plasma in a sluggish fashion '<ref>OMIM.Omim.org/entry/107741.</ref>'. '<references/>' | Prevention of Atherosclerosis Using Adenovirus Vectors. The Journal of Clinical Investigation 96:1612-1620.</ref>'. Individuals homozygous for the ε2 allele are most susceptible. The E2 isoform of apoE exhibits weak or defective binding of remnants to hepatic lipoprotein receptors; the E2 isoform also clears these remnants from the plasma in a sluggish fashion '<ref>OMIM.Omim.org/entry/107741.</ref>'. | ||
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==References== | |||
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