Galectin-lattice sustains function of cationic amino acid transporter and insulin secretion of pancreatic β cells.

摘要: Maintenance of cell surface residency and function glycoproteins by lectins are essential for regulating cellular functions. Galectins β-galactoside-binding form a galectin-lattice, which regulates stability, clustering, membrane sub-domain localization endocytosis plasmalemmal glycoproteins. We have previously reported that galectin-2 (Gal-2) forms complex with cationic amino acid transporter 3 (CAT3) in pancreatic β cells, although the biological significance molecular interaction between Gal-2 CAT3 has not been elucidated. In this study, we demonstrated structure N-glycan was either tetra- or tri-antennary branch carrying β-galactosides, works as galectin-ligands. Indeed, bound to using β-galactoside epitope. Moreover, disruption glycan-mediated bindings galectins significantly reduced expression levels CAT3. The attenuated arginine uptake activities subsequently nitric oxide production, thus impaired arginine-stimulated insulin secretion cells. These results indicate galectin-lattice stabilizes preventing sustain This provides novel insight into endocrinological mechanism nutrition metabolism homeostasis.