When the blood sugar level falls between meals the liver converts glycogen to glucose and releases it back into the bloodstream to be used as fuel and to keep the blood sugar from falling too low. When food is eaten and the blood sugar rises, causing insulin to be released into the blood it signals the liver to stop converting glycogen into glucose, and to begin drawing the excess glucose from the blood to rebuild its glycogen stores. Each cell is surrounded by a membrane, called the sarcolemma. The sarcolemma is the part of the muscle which contracts. The defect in HypoKPP is in a specific voltage-gated ion channel, depending on the mutation.
Ion channels are small pores which pierce the sarcolemma.
Most ion channels will admit only one type of ion, and some will only accept an ion only when it is in a specific state. Patients with any form of periodic paralysis have a lowered resting membrane potential during attacks. This is what causes the paralysis or weakness. The role of insulin is more than just provocative. It appears that there may be an abnormal sensitivity to insulin in HypoKPP patients.