Modulation of IKK/NF-B signaling iin pancreatic ß-cells induces diabetes
Auch gedruckt in der BibliothekW: W-H 13.436
FakultätFakultät für Naturwissenschaften
Ressourcen- / MedientypDissertation, Text
Datum der Freischaltung2013-11-19
Inflammation has been reported to be involved in obesity and insulin resistance as well as type 1 and type 2 Diabetes (T1D, T2D). In the course of both T1D and T2D, insulin-producing beta-cells in pancreatic islets are known to be finally destroyed by different molecular mechanisms. The IKK2/NF-kappa B system is the master regulator of inflammatory processes. The contribution of IKK/NF-kappa B signaling in this context is controversially discussed and ranges from pro- to anti-apoptotic functions in the regulation of beta-cell survival. To address this issue we generated conditional loss- and gain-of-function mouse models to manipulate IKK activity specifically in beta-cells. Both, inhibition and constitutive activation of IKK2/NF-kappa B signaling results in hyperglycemia and reduction of beta-cell mass indicating a critical role of balanced IKK signaling in beta-cell homeostasis.
Nuklearfaktor Kappa B
Freie SchlagwörterB signaling