Respuesta :
A homozygous mutation will result in the complete absence of LDL receptors on hepatocytes, increasing the LDL cholesterol levels. The correct answer is option (A).
Very low-density lipoprotein (VLDL) is produced by the liver and converted to IDL by lipoprotein lipase (LPL). By means of hepatic triglyceride lipase, IDL gets changed into LDL (HTGL). Hypercholesterolemia, also referred to as familial hypercholesterolemia, is an autosomal dominant illness that can be brought on by defects in LDL receptor function. Because the binding and subsequent uptake of LDL molecules in the blood depends on LDL receptors on the surface of hepatocytes, a hereditary decrease in LDL receptor number would result in a lower ability of hepatocytes to absorb LDL and increase LDL in the blood. LDL is typically around 300 mg/dL, but if this mutation is heterozygous, some LDL receptors will be present in the hepatocytes. The LDL cholesterol levels will rise to 1000 mg/dL due to the complete absence of LDL receptors on hepatocytes as a result of a homozygous mutation, though.
The complete question is:
What type(s) of mutation(s) would result in the inability of an individual’s cells to take up LDL from the bloodstream?
(A). Mutations could occur in the receptor itself to preclude LDL binding.
(B). Mutations could occur in proteins that position the LDL receptor on the plasma membrane.
(C). Mutations could occur in the protein machinery that allows the LDL particle to enter the cell.
(D). Mutations could occur in the protein component of LDL that recognizes the receptor.
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