This site is intended for healthcare professionals

Sign in
Go to /sign-in page

You can view 5 more pages before signing in

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.

Create an account to add page annotations

Create a free account

Annotations allow you to add information to this page that would be handy to have on hand during a consultation. E.g. a website or number. This information will always show when you visit this page.

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.

Connect

Copyright 2024 Oxbridge Solutions Limited, a subsidiary of OmniaMed Communications Limited. All rights reserved. Any distribution or duplication of the information contained herein is strictly prohibited. Oxbridge Solutions receives funding from advertising but maintains editorial independence.