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题名:SMAD2 disruption in mouse pancreatic beta cells leads to islet hyperplasia and impaired insulin secretion due to the attenuation of ATP-sensitive K channel activity.
作者:NOMURA M; ZHU HL; WANG L; MORINAGA H; TAKAYANAGI R; TERAMOTO N;
来源:Diabetologia. 2013 Sep 26. [ IF= 6.49 ] ]
URL :10.1007/s00125-013-3062-2
日期:20131002
摘要:AIMS/HYPOTHESIS: The TGF-beta superfamily of ligands provides important signals
for the development of pancreas islets. However, it is not yet known whether the
TGF-beta family signalling pathway is required for essential islet functions in
the adult pancreas. METHODS: To identify distinct roles for the downstream
components of the canonical TGF-beta signalling pathway, a Cre-loxP system was
used to disrupt SMAD2, an intracellular transducer of TGF-beta signals, in
pancreatic beta cells (i.e. Smad2beta knockout [KO] mice). The activity of
ATP-sensitive K+ channels (KATP channels) was recorded in mutant beta cells using
patch-clamp techniques. RESULTS: The Smad2betaKO mice exhibited defective insulin
secretion in response to glucose and overt diabetes. Interestingly, disruption of
SMAD2 in beta cells was associated with a striking islet hyperplasia and
increased pancreatic insulin content, together with defective glucose-responsive
insulin secretion. The activity of KATP channels was decreased in mutant beta
cells. CONCLUSIONS/INTERPRETATION: These results suggest that in the adult
pancreas, TGF-beta signalling through SMAD2 is crucial for not only the
determination of beta cell mass but also the maintenance of defining features of
mature pancreatic beta cells, and that this involves modulation of KATP channel
activity.

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