Genotype‐Dependent Functional and Pharmacological Profiling of Rare GCK Variants Reveals Implications for Precision Management of Monogenic Diabetes

Abstract

Rare GCK variants contribute to heterogeneous forms of monogenic diabetes, yet the molecular basis underlying their diverse functional consequences and pharmacological responsiveness remains incompletely understood. As glucokinase (GCK) serves as a central glucose sensor in pancreatic β‐cells and hepatocytes, defining the functional properties of individual variants may improve molecular diagnosis and inform the interpretation of potential therapeutic responses in GCK‐maturity‐onset diabetes of the young (GCK‐MODY, also called MODY2).