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The primary biochemical lesion in homozygote with familial hypercholesterolemia (type IIa) is 

(A) Loss of feed back inhibition of HMG reductase 

(B) Loss of apolipoprotein B 

(C) Increased production of LDL from VLDL 

(D) Functional deficiency of plasma membrane receptors for LDL

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(D) Functional deficiency of plasma membrane receptors for LDL

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