Log in first for optimal use of all functions!

    Phosphorylation of TXNIP by AKT Mediates Acute Influx of Glucose in Response to Insulin (Unknown language)

    Free access
    In: Cell Reports, Vol 19, Iss 10, Pp 2005-2013 (2017) ; 2017
    • ISSN:
      2211-1247
    • Article (Journal)  /  Electronic Resource

    How to get this title?

    Download

    Export, share and cite

    Growth factors, such as insulin, can induce both acute and long-term glucose uptake into cells. Apart from the rapid, insulin-induced fusion of glucose transporter (GLUT)4 storage vesicles with the cell surface that occurs in muscle and adipose tissues, the mechanism behind acute induction has been unclear in other systems. Thioredoxin interacting protein (TXNIP) has been shown to be a negative regulator of cellular glucose uptake. TXNIP is transcriptionally induced by glucose and reduces glucose influx by promoting GLUT1 endocytosis. Here, we report that TXNIP is a direct substrate of protein kinase B (AKT) and is responsible for mediating AKT-dependent acute glucose influx after growth factor stimulation. Furthermore, TXNIP functions as an adaptor for the basal endocytosis of GLUT4 in vivo, its absence allows excess glucose uptake in muscle and adipose tissues, causing hypoglycemia during fasting. Altogether, TXNIP serves as a key node of signal regulation and response for modulating glucose influx through GLUT1 and GLUT4.

    Metadata by DOAJ is licensed under ​CC BY-SA 1.0

    How to get this title?

    Download

    Export, share and cite

    Feedback