Glucose Transport

Glucose is polar and can't cross the lipid bilayer unassisted — it needs GLUT transporter proteins. GLUT2 and GLUT4 are the two MCAT-relevant isoforms.
GLUT2 (liver, pancreatic beta cells): high Km (~15 mM, above normal blood glucose ~5.5 mM) → low affinity, active mainly when glucose is elevated. Pairs with glucokinase as a glucose sensor in beta cells.
GLUT4 (skeletal muscle, adipose tissue): Km close to normal blood glucose (~5 mM) → high responsiveness. Insulin-dependent — insulin triggers exocytosis of GLUT4 into the membrane; falling insulin triggers endocytosis back into vesicles.
Post-meal sequence: blood glucose rises → GLUT2 lets glucose into beta cells → insulin secreted → GLUT4 translocates to muscle/fat membranes → glucose uptake increases → blood glucose normalizes.

GLUT2: Low-affinity (high Km) glucose transporter in liver and pancreatic beta cells; acts as a glucose sensor, not insulin-dependent.
GLUT4: High-affinity (Km ~ normal glucose) glucose transporter in muscle/adipose tissue; insulin-dependent membrane insertion.
Km: Substrate concentration at half-maximal transport rate — inverse proxy for affinity (low Km = high affinity).

Feature	GLUT2 vs. GLUT4
Tissue	Liver, pancreatic beta cells / Skeletal muscle, adipose tissue
Km for glucose	High (~15 mM) / Close to normal (~5 mM)
Affinity	Low / High (relative to normal glucose)
Insulin-dependent?	No / Yes — insulin drives membrane insertion (exocytosis)
Role	Glucose sensor (with glucokinase) / Insulin-responsive uptake

1Blood glucose rises after a meal.
2Elevated glucose enters pancreatic beta cells via GLUT2 (low-affinity, activates only when glucose is high).
3Rising intracellular glucose in beta cells triggers insulin secretion.
4Insulin signals muscle/adipose tissue to move GLUT4 vesicles to the membrane via exocytosis.
5Glucose uptake into muscle/fat increases; blood glucose returns to normal.

GLUT2's high Km makes it a poor everyday transporter but a great sensor — don't assume high Km = 'better' transporter; it means the opposite of high affinity.
GLUT4 moves via insulin-triggered exocytosis (into membrane) and endocytosis (out of membrane) — direction matters: rising insulin = more GLUT4 in the membrane.

Why does GLUT2's high Km make it a good glucose sensor in beta cells?

What triggers GLUT4 to move to the plasma membrane?

Which two tissues express GLUT2?

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