a. Indirectly stimulating LDL uptake through HMG-CoA reductase inhibition and LDL receptor upregulation.
b.
Increasing bile salt production as a consequence of higher cholesterol availability.
c. Potentially impacting intestinal cholesterol synthesis through improved fat absorption by bile salts.
a) Rate at which liver cells import cholesterol:
Statins inhibit HMG-CoA reductase, reducing its activity. HMG-CoA reductase is crucial for converting a molecule called HMG-CoA into mevalonate, a building block for cholesterol. With less HMG-CoA reductase activity, mevalonate production decreases. Lower mevalonate levels trigger a compensatory mechanism in the liver cells.
b) Rate at which enzymes in the liver convert cholesterol into bile salts:
The increased uptake of LDL cholesterol by the liver provides more substrate for bile salt production.
Bile salts are important for digestion and fat absorption.
Enzymes in the liver, primarily cholesterol 7α-hydroxylase, convert cholesterol into bile salts.
With abundant cholesterol available, bile salt production is stimulated.
Therefore, the rate of cholesterol conversion into bile salts increases.
c) Concentration of LDL cholesterol in the blood:
Enhanced LDL uptake by the liver due to upregulated receptors removes LDL cholesterol from the circulation which decreases the overall concentration of LDL cholesterol in the blood. Increased bile salt production can indirectly contribute to lowered LDL levels. Bile salts help emulsify fats in the intestine, promoting their absorption.