Glucose transporter type 2 (GLUT2) is a well known cellular component responsible for glucose-stimulated insulin secretion within pancreatic β-cells. Low levels of this transporter are linked to development of type 2 diabetes, and it is known that glucocorticoids are involved in pancreatic β-cell destruction. However, the link between the two has not yet been uncovered.

Ono and Kataoka investigated the role of hepatocyte nuclear factor-1 (HNF1), a transcription factor normally seen regulating gene activity in the liver and pancreas, among others, in linking glucocorticoid usage and GLUT2 reduction. Using a comprehensive in vitro approach, they clearly demonstrated that mRNA expression of the gene responsible for GLUT2 proteins (Slc2a2) is reduced by the application of dexamethasone in glucose-responsive cells, and that this repression is solely due to HNF1α or HNF1β.

This study opens up the potential for understanding the progression of type 2 diabetes in some patients, whilst also providing new evidence for future studies in the area.

Read the full article in Journal of Molecular Endocrinology 74 e240077 https://doi.org/10.1530/JME-24-0077