Glucose-stimulated insulin secretion (GSIS) involves cross talk between small Gproteins and their regulating factors. These interactions results in translocation of insulin-laden granules to the plasma membrane for fusion and insulin release. Vesicular transport and fusion events are tightly regulated by signals which coordinate between vesicle-and membrane-associated docking proteins. It is now being accepted that small G-protein, Rac1-mediated Reactive Oxygen Species (ROS) functions as a second messenger in islet β-cell function. Further, evidence from multiple laboratories suggests a tonic increase in ROS generation is necessary for GSIS and fatty acid-induced insulin secretion. On the other hand, Rac1-mediated NADPH oxidase-activation and subsequent generation of excessive ROS under glucolipotoxic conditions and cytokines exposure has proven to be detrimental for islet β-cell function. In this review we overview the normal physiological effects (positive role) and adverse effects (negative role) of activated small G-protein, Rac1 in pancreatic β-cells.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.