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Joined 2026-09-21 Message
Incoming links: Hyperinsulinism
Benjamin Glaser Created 2026-10-20 Updated 2026-11-05
Researcher in metabolic disease. Glaser and collaborators identified an activating glucokinase mutation associated with familial hyperinsulinism, connecting altered glucose sensing with inappropriate insulin release.[ref]
Familial Hyperinsulinism Caused by an Activating Glucokinase Mutation by Benjamin Glaser and others. Title, author list and reported study
Hyperinsulinism 2026-11-05
Hyperinsulinism is excessive or inappropriately sustained insulin action or secretion for the metabolic context. In hyperinsulinaemic hypoglycaemia, insulin secretion is insufficiently suppressed as blood glucose falls. Insulin promotes glucose utilization and storage while restraining endogenous glucose production, so the combination can lower the circulating glucose supply. [ref]
Familial Hyperinsulinism Caused by an Activating Glucokinase Mutation by Benjamin Glaser and others. 1998, familial mutation, increased glucokinase activity and altered glucose sensing
The activating glucokinase mutation provides a mechanistic example: changing the beta-cell glucose-sensing system shifts the conditions under which insulin is released. A measured insulin concentration must therefore be interpreted alongside the simultaneous glucose state. A concentration that is unremarkable after a meal can be inappropriate during hypoglycaemia; a single universal numerical cutoff does not describe the whole mechanism.