Open AccessKATPChannel Closure Ameliorates the Impaired Insulinotropic Effect of Glucose-Dependent Insulinotropic Polypeptide in Patients with Type 2 Diabetes
Author(s) -
Kasper Aaboe,
Filip K. Knop,
Tina Vilsbøll,
Aage Vølund,
Ulf Simonsen,
Carolyn F. Deacon,
Sten Madsbad,
Jens J. Holst,
Thure Krarup
Publication year - 2008
Publication title -
the journal of clinical endocrinology and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.206
H-Index - 353
eISSN - 1945-7197
pISSN - 0021-972X
DOI - 10.1210/jc.2008-1731
Subject(s) - medicine , endocrinology , incretin , gastric inhibitory polypeptide , insulin , type 2 diabetes , diabetes mellitus , glipizide , glucagon like peptide 1 , hormone , glucagon , glucose clamp technique , pancreatic hormone , insulin resistance
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.
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