Endoplasmic reticulum stress causes insulin resistance by inhibiting delivery of newly synthesized insulin receptors to the cell surface

Abstract

Endoplasmic reticulum (ER) stress inhibits activation of AKT by insulin by depleting insulin receptors and interferes with the delivery of newly synthesized insulin receptors to the cell surface. Bypass of the secretory pathway in synthesis of the cytosolic protein tyrosine kinase domain of the insulin receptor negates the effects of ER stress on activation of AKT by insulin.