Lipoprotein uptake function

ApoC-I is expressed mainly in liver but also in lung, skin, testis, spleen, neural retina, and RPE. Its multiple functions include the activation of lecithin cholesterol acyltransferase (LCAT) and the inhibition, among others, of lipoprotein and hepatic lipases that hydrolyze triglycerides in particle cores. Notably, both LCAT and lipoprotein lipases are expressed in RPE and choroid (Li et al., 2006). Moreover ApoC-I has been shown to displace ApoE on the VLDL and LDL and thus hinder their binding and uptake via their corresponding receptors (Li et al., 2006). 

The answer is a. (Katzung, p 590.) Bile acids are absorbed primarily in the ileum of the small intestine. Cholestyramine binds bile acids, preventing their reabsorption in the jejunum and ileum. Up to 10-fold greater excretion of bile acids occurs with the use of resins. The increased clearance leads to increased cholesterol turnover of bile acids. Low-density lipoprotein receptor upregulation results in increased uptake of LDL. This does not occur in homozygous familial hypercholesterolemia because of lack of functioning receptors. 

The major function of LTP-I in human plasma may be to distribute es-terified cholesterol from the HDL fraction, where cholesterol is esterified, to other lipoprotein fractions. LCAT activity is responsible for the production of some 50-100 nmol esterified cholesterol per milliliter of plasma per hour (Gil). The concentration of esterified cholesterol in human HDL is about 1000 nmol/ml of plasma. Only 0.5-1.0% of HDL apoprotein is removed from plasma per hour (B41), probably mainly in intact HDL particles. If so, then the uptake of HDL particles can account for the removal from plasma of only about 10-20% of the esterified cholesterol formed in HDL in the LCAT reaction. 

The liver has a variety of functions in lipid metabolism (7.) uptake, oxidation and transformation of free fatty acids, (2.) synthesis of plasma lipoproteins, (3.) trans-... 

Neurons rely upon a ready supply of cholesterol for maintaining a broad array of physiological functions such as membrane synthesis, myeUn maintenance, electrical signal transduction, synaptic transmission, and plasticity. Cholesterol metabolism in the CNS is unique compared with the rest of the body. Because of the existence of the blood-brain barrier (BBB), almost all the sterol required for new membranes comes from de novo synthesis within the CNS [33]. In addition, the brain has evolved highly efficient mechanisms to maximize the utihzation of cholesterol. UnUke other membrane lipid components, cholesterol cannot be synthesized at neuronal terminals. Therefore, synaptic function depends largely on cholesterol supplied from either axonal transport from the cell body and or uptake of Upidated ApoE produced by astroglia via neuronal lipoprotein receptors. 

While the LDL pathway for control of cholesterol uptake was elucidated using cultured cells, it also appears to be functional in vivo. The pattern of regulation depicted in Fig. 5 has been confirmed in freshly isolated blood leukocytes and lymphocytes [89-92]. In addition, administration of 4-aminopyrazolepyrimidine, a drug which suppresses lipoprotein release from animal liver [93], elevates HMG-CoA reductase levels and cholesterol synthesis in non-hepatic tissues [94,95]. These observations are consistent with the hypothesis that non-hepatic cells exhibit a low rate of cholesterol synthesis because they utilize cholesterol synthesized by the liver and present in the plasma lipoproteins [96],... 

---