Hypoglycaemia counter-regulation

Hypoglycaemia triggers glucagon-driven hepatic glucose release that returns blood glucose to setpoint. An insulin overdose drives glucose down to a nadir of 4.6–3.5 mM with increasing challenge; the finite hepatic glycogen buffer (the liver/HHEX role) then restores ~5 mM without overshoot. The bounded counter-regulatory loop is forced [V]; the glycogen capacity is a model unit [O].

An α-cell population of R19 switches raises hepatic glucose production when glucose falls; insulin-overdose nadirs of 4.6–3.5 mM recover to ~5 mM, bounded below 9 mM on rebound. The loop is forced [V]; the absolute glycogen capacity is a model unit, graded [O] with a stated obstacle.

Hypoglycaemia triggers glucagon-driven hepatic glucose release that returns blood glucose to setpoint without overshoot. An insulin overdose drives glucose to a nadir between 4.6 and 3.5 mM as the challenge grows, after which the loop restores ~5 mM.

The counter-regulatory arm is the mirror of the insulin arm: a population of α-cell R19 switches turns on when glucose falls, raising hepatic glucose production. The finite hepatic glycogen store (the liver / HHEX role) is the buffer that is drawn down to supply this release, which is why recovery is bounded.

The bounded counter-regulatory loop is forced [V]; the absolute glycogen capacity is a model unit, not a physiological mass, and is therefore graded [O] with the obstacle stated in the irreproducibility ledger. The loop never diverges — glucose stays below 9 mM on rebound — because the buffer is finite.