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(2020) 8:e000695
Psychiatry 32 , 117127 (2024)
The Bioavailability Breakthrough: Liposomal Delivery To address the issues of absorption and stomach discomfort, researchers developed liposomal delivery
The GLP-1R has been previously reported to follow a dynamin-dependent, but either clathrin-mediated (CME) or clathrin-independent (CIE) endocytosis pathway ( via clathrin-coated pits ( via clathrin-coated pits in pancreatic beta cells ( via interaction with the 2 subunit of the AP2 clathrin adaptor, promoting movement of the GPCR--arrestin complex to vesicular pits where -arrestin, AP2 and clathrin form a tripartite interaction ( In contrast to the above evidence supporting primarily a CME-dependent endocytosis pathway, experiments with small interfering RNA targeting clathrin did not appear to affect GLP-1R endocytosis in HEK293 cells, suggesting the existence of an alternative CIE-mediated mechanism ( q proteins, followed by activation of PKC ( The Role of Membrane Nanodomains in GLP-1R Endocytosis The local organisation of GPCRs within plasma membrane cholesterol- and sphingolipid-enriched nanodomains (historically known as liquid-ordered domains or lipid rafts) can be dynamically regulated by ligand-induced activation, and is a key regulator of GPCR behaviours through compartmentalisation of both receptor and signalling effectors into membrane hotspots ( s , the main G protein signalling subunit for the GLP-1R, was predominantly associated with cholesterol-rich detergent-resistant membrane fractions in beta cells ( via either clathrin-dependent and clathrin-independent pathways, as demonstrated by the virtual abolition of agonist-induced GLP-1R internalisation following cholesterol extraction with MCD (methyl--cyclodextrin) in beta cells ( Post-Endocytic GLP-1R Sorting/Trafficking Post-endocytic GPCR trafficking occurs through a series of dynamically interconnected organelles crucial for the sorting of receptors to different intracellular compartments ( via a short/fast cycle of trafficking from a Rab5-positive to a Rab4-positive endocytic compartment, via a long/slow cycle by entering Rab11-positive perinuclear recycling endosomes, or towards lysosomal degradation via retention in intraluminal vesicles (ILVs) of multivesicular bodies (MVBs), generated by maturation of EEs, a process that also causes termination of signalling, and subsequent trafficking to Rab7-positive late endosomes and lysosomes ( Once internalized, the acidic endosomal pH disrupts ligand-receptor interactions and influences post-endocytic GPCR trafficking, presumably as ligand-bound versus apo-state GPCR conformations show altered engagement, directly or indirectly, with local trafficking effectors
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