Phosphorylation of TXNIP by AKT Mediates Acute Influx of Glucose in Response to Insulin Academic Article uri icon


MeSH Major

  • Antioxidants
  • Blood Proteins
  • Diabetes Mellitus, Experimental
  • Diabetes Mellitus, Type 2
  • Insulin-Secreting Cells


  • 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.

publication date

  • June 6, 2017



  • Academic Article



  • eng

PubMed Central ID

  • PMC5603216

Digital Object Identifier (DOI)

  • 10.1016/j.celrep.2017.05.041

PubMed ID

  • 28591573

Additional Document Info

start page

  • 2005

end page

  • 2013


  • 19


  • 10