KATP channel closure ameliorates the impaired insulinotropic effect of glucose-dependent insulinotropic polypeptide in patients with type 2 diabetes

Kasper Aaboe, Filip Krag Knop, Tina Vilsbøll, Aage Vølund, Ulf Simonsen, Carolyn Fiona Deacon, Sten Madsbad, Jens Juul Holst, Thure Krarup

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Abstract

The reduced incretin effect in subjects with type 2 diabetes is accompanied by a severely impaired insulinotropic effect of the incretin hormone glucose-dependent insulinotropic polypeptide (GIP). The K(ATP) channels of the beta-cell appear to be essential for the function of GIP in mice, and mutations in the gene encoding these channels have been linked to the development of type 2 diabetes. With this study we therefore aimed at clarifying the role of K(ATP) channel malfunction in the impaired function of GIP.
OriginalsprogEngelsk
TidsskriftJournal of Clinical Endocrinology and Metabolism
Vol/bind94
Udgave nummer2
Sider (fra-til)603-8
Antal sider6
ISSN0021-972X
DOI
StatusUdgivet - 1 feb. 2009

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