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Pathogenesis

Last reviewed dd mmm yyyy. Last edited dd mmm yyyy

Authoring team

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.

Reference:

  • Ashcroft, FM. (1996). Sweet news for hypoglycaemic babies. Nature Medicine, 2(12), 1301-2.
  • Kane, C. et al. (1996). Loss of functional K-ATP channels in pancreatic beta-cells causes persistent hyperinsulinemic hypoglycaemia of infancy. Nature Medicine, 2(12), 1344-7.

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The content herein is provided for informational purposes and does not replace the need to apply professional clinical judgement when diagnosing or treating any medical condition. A licensed medical practitioner should be consulted for diagnosis and treatment of any and all medical conditions.

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