Dysregulation of the TRIO-ELMO2-CSNK1G2 Axis Impairs GLUT4 Translocation in Type 2 Diabetes

Abstract

This study investigates the roles of TRIO, ELMO2, and CSNK1G2 in the context of type 2 diabetes by analyzing publicly available gene expression datasets derived from insulin-resistant human skeletal muscle. Our analysis reveals a pronounced downregulation of these genes, each of which encodes proteins involved in key cellular processes: TRIO in cytoskeletal remodeling, ELMO2 in Rac1-mediated signaling, and CSNK1G2 in vesicle trafficking. Based on these findings, we propose the existence of a coordinated regulatory mechanism—referred to here as the TRIO–ELMO2–CSNK1G2 axis—which appears to be critical for insulin-stimulated translocation of GLUT4 to the plasma membrane. The observed suppression of this axis may underlie defects in glucose uptake and contribute to the development of insulin resistance. These insights highlight a potentially novel therapeutic target for the treatment of type 2 diabetes.