The Km value in glucose transporters represents:
Facilitative transporters follow Michaelis-Menten-like saturation where velocity depends hyperbolically on concentration. Km operationally defined as substrate concentration where transport rate equals half Vmax maximal rate when all carriers saturated cycling at turnover. It serves as inverse affinity measure: low Km around one millimolar indicates high affinity because half maximal achieved at low concentration suitable for tissues needing glucose despite hypoglycemia typical for GLUT3 in neurons and GLUT1 in erythrocytes. High Km around fifteen to twenty millimolar indicates low affinity where rate responds linearly across physiological range without early saturation behaving as sensor as in GLUT2 in hepatocytes, beta cells and basolateral enterocytes matching blood changes. Km is intrinsic property reflecting pocket complementarity and dynamics independent of transporter number. Changes in Vmax reflect altered expression or translocation while altered Km suggests missense affecting binding as in Fanconi-Bickel with GLUT2 mutations raising apparent Km. Understanding Km aids predicting tissue handling metabolic flux and insulin secretion coupling that depends on high Km glucokinase, allowing proportional regulation and glucose sensing in liver and pancreas for homeostasis.
Ref: Mueckler & Thorens, Molecular Aspects of Medicine 2013: Glucose Transporters – Km as Half-Vmax Concentration.