详细记录  
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. 2014 Jan;57(1):157-66. doi: 10.1007/s00125-013-3062-2. Epub 2013 [ IF= 6.49 ] ]
URL :10.1007/s00125-013-3062-2
日期:20140217
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.

================  评  论  部  分=================

重要性:
分类:(参照 Faculty of 1000 的分类体系)


评语:

评论密码:   返回前页  [全部]