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#phosphatidylcholine

2 public questions tagged with this topic.

Which of the following is true for phosphatidylcholine?

Phosphatidylcholine dominates eukaryotic membranes, constituting 40-50% of total phospholipid, existing as zwitterion at neutral pH with positively charged trimethylammonium and negatively charged phosphate, yielding net neutral molecule that stabilizes lamellar bilayer phase and prevents excessive electrostatic repulsion between headgroups. Its cylindrical molecular geometry with roughly equal cross-section of headgroup and two acyl chains favors planar bilayer formation, contrasting cone-shaped PE that induces curvature. Physiologically outstanding example is lung surfactant synthesized by type II alveolar cells in lamellar bodies containing dipalmitoylphosphatidylcholine DPPC with two saturated palmitate chains plus surfactant proteins SP-B and SP-C; DPPC reduces alveolar surface tension to near zero at end-expiration, preventing alveolar collapse and decreasing work of breathing. Premature infants deficient in surfactant develop respiratory distress syndrome treated with exogenous surfactant replacement therapy. In plasma membrane outer leaflet, PC serves as reservoir for signaling lipid phosphatidic acid via phospholipase D and as substrate for sphingomyelin synthesis, illustrating structural and metabolic versatility beyond membrane structure.

Ref: Lodish et al., Molecular Cell Biology, 9th ed., Chapter 10: Phosphatidylcholine and Pulmonary Surfactant.

Which ABC transporter is found in the liver and is responsible for phosphatidylcholine transport?

Hepatic bile secretion relies on coordinated action of several canalicular ABC transporters in hepatocytes. ABCB11 BSEP exports bile acids, ABCG5/ABCG8 heterodimer exports cholesterol, and ABCB4 previously called MDR2 in mice and MDR3 in humans is dedicated to phosphatidylcholine. ABCB4 acts as ATP-dependent floppase moving phosphatidylcholine from inner cytoplasmic leaflet to outer exoplasmic leaflet of canalicular membrane where bile salt micelles extract it into biliary space forming mixed micelles. This phospholipid shield protects cholangiocyte membranes from detergent attack by hydrophobic bile salts and solubilizes cholesterol preventing crystal formation. Mice lacking Abcb4 develop spontaneous cholangitis, bile duct proliferation, and biliary fibrosis due to regurgitation of low-phospholipid toxic bile. In humans, biallelic loss causes progressive familial intrahepatic cholestasis type 3 presenting in childhood, while heterozygous variants predispose to low-phospholipid-associated cholelithiasis, intrahepatic cholestasis of pregnancy and drug-induced cholestasis, demonstrating essential protective role in hepatic physiology. Such detailed mechanistic insight is frequently examined in competitive tests including NEET, CUET, CSIR-NET and GATE where transporter classification, energetics and disease linkage are integrated into problem-solving questions.

Ref: Oude Elferink & Paulusma, Pflugers Arch 2007, ABCB4 bile phospholipid secretion.