Chronic exposure to KATP channel openers results in attenuated glucose sensing in hypothalamic GT1-7 neurons
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- 作者：Elizabeth Haythorne e.haythorne@imperial.ac.uk" class="auth_mail" title="E-mail the corresponding author ; D. Lee Hamilton d.l.hamilton@stir.ac.uk" class="auth_mail" title="E-mail the corresponding author ; John A. Findlay J.A.Findlay@soton.ac.uk" class="auth_mail" title="E-mail the corresponding author ; Craig Beall C.Beall@exeter.ac.uk" class="auth_mail" title="E-mail the corresponding author ; Rory J. McCrimmon r.mccrimmon@dundee.ac.uk" class="auth_mail" title="E-mail the corresponding author ; Michael L.J. Ashford ; m.l.j.ashford@dundee.ac.uk" class="auth_mail" title="E-mail the corresponding author
- 关键词：NN414 ; Diazoxide ; KATP ; Glucose sensing ; Hypoglycemia ; Type 1 diabetes
- 刊名：Neuropharmacology
- 出版年：2016
- 出版时间：December 2016
- 年：2016
- 卷：111
- 期：Complete
- 页码：212-222
- 全文大小：3014 K
文摘
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Chronic exposure to NN414 blunts hypoglycaemic responses in GT1-7 neurons.
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NN414 does not cause adaptations in glucose metabolism.
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The availability of KATP to open is greatly diminished by NN414.
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Preventing NN414 binding or conformation change to KATP rescues channel activity.