In the case of LDL-receptor deficiency, which protein would be upregulated as a result of statin therapy?

In the context of LDL-receptor deficiency, statin therapy is known to decrease cholesterol synthesis in the liver, primarily by inhibiting the enzyme HMG-CoA reductase. As a result of reduced intracellular cholesterol levels, the liver responds by increasing the expression of LDL receptors on its surface. The upregulation of LDL receptors enhances the uptake of low-density lipoprotein (LDL) particles from the bloodstream, which helps lower plasma LDL cholesterol levels.

This mechanism is particularly important in patients with LDL-receptor deficiency, where the fundamental issue is a reduced ability to clear LDL cholesterol from the blood. By promoting the synthesis and expression of LDL receptors, statins can partially overcome the impaired clearance of LDL, providing therapeutic benefits despite the underlying deficiency.

The other options—cholesterol acyltransferase, lipoprotein lipase, and hepatic lipase—are involved in different aspects of lipid metabolism but do not directly respond to statin therapy in the same way that LDL receptors do. Therefore, the correct answer is that statin therapy leads to upregulation of the LDL receptor.