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Article

Glucose-Sensitive CFTR Suppresses Glucagon Secretion by Potentiating KATP Channels in Pancreatic Islet α Cells.

Endocrinology - 1 Oct 2017

Huang Wen Qing, Guo Jing Hui, Zhang Xiao Hu, Yu Mei Kuen, Chung Yiu Wa, Ruan Ye Chun, Chan Hsiao Chang

Abstract excerpt

The secretion of glucagon by islet α cells is normally suppressed by high blood glucose, but this suppressibility is impaired in patients with diabetes or cystic fibrosis (CF), a disease caused by mutations in the gene encoding CF transmembrane conductance regulator (CFTR), a cyclic adenosine monophosphate-activated Cl- channel. However, precisely how glucose regulates glucagon release remains controversial. Here...

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Identifiers

PMID: 28977595
DOI: 10.1210/en.2017-00282

Genes

CFTR

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Glucose-Sensitive CFTR Suppresses Glucagon Secretion by Potentiating KATP Channels in Pancreatic Islet α Cells.PMID 28977595Read ↗

CFTR is involved in the regulation of glucagon secretion in human and rodent alpha cells.Semantic proximity Read ↗

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The role of mu-opioid receptors in pancreatic islet alpha cellsSemantic proximity Read ↗

Membrane depolarization and calcium influx induce glucagon gene transcription in pancreatic islet cells through the cyclic AMP-responsive element.Semantic proximity Read ↗

The ablation of the Ca(v)2.3/E-type voltage-gated Ca2+ channel causes a mild phenotype despite an altered glucose induced glucagon response in isolated islets of Langerhans.Semantic proximity Read ↗

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Targeted overactivity of beta cell K(ATP) channels induces profound neonatal diabetes.Semantic proximity Read ↗

Cystic fibrosis-related diabetes is caused by islet loss and inflammation.Semantic proximity Read ↗

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