Abstract
Oversupply of free fatty acids such as palmitic acid (PA) from the portal vein may cause liver insulin resistance. Production of reactive oxygen species plays a pivotal role in PA‐induced insulin resistance in H4IIEC3 hepatocytes. Recently, we found that exosomes secreted from INS‐1 cells that were transfected with neutral ceramidase (NCDase) plasmids had raised NCDase activity; these NCDase‐enriched exosomes could inhibit PA‐induced INS‐1 cell apoptosis. Here, we showed that PA reduced insulin‐stimulated tyrosine phosphorylation of insulin receptor substrate 2 and decreased insulin‐stimulated uptake of the fluorescent glucose analog 2‐NBDG, confirming that insulin resistance occurred in PA‐treated H4IIEC3 cells. Moreover, NCDase‐enriched exosomes from INS‐1 cells rescued PA‐induced H4IIEC3 insulin resistance and blocked PA‐induced reactive oxygen species production in which ceramide was involved.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
