Familial forms of PHHI have been linked to mutations in the gene encoding the regulatory subunit of the beta-cell ATP-sensitive potassium channel.
The ATP-sensitive potassium channel closes when the blood glucose level is high resulting in depolarisation of the beta-cell membrane, an influx of calcium and the consequent release of insulin.
Cases of PHHI show no ATP-sensitive potassium channel activity and hence continually secrete insulin without regard to the blood glucose.
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