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- W2064286821 abstract "Pulsatile secretion is an inherent property of hormone-releasing pancreatic islet cells. This secretory pattern is physiologically important and compromised in diabetes. Neurotransmitters released from islet cells may shape the pulses in auto/paracrine feedback loops. Within islets, glucose-stimulated β-cells couple via gap junctions to generate synchronized insulin pulses. In contrast, α- and δ-cells lack gap junctions, and glucagon release from islets stimulated by lack of glucose is non-pulsatile. Increasing glucose concentrations gradually inhibit glucagon secretion by α-cell-intrinsic mechanism/s. Further glucose elevation will stimulate pulsatile insulin release and co-secretion of neurotransmitters. Excitatory ATP may synchronize β-cells with δ-cells to generate coinciding pulses of insulin and somatostatin. Inhibitory neurotransmitters from β- and δ-cells can then generate antiphase pulses of glucagon release. Neurotransmitters released from intrapancreatic ganglia are required to synchronize β-cells between islets to coordinate insulin pulsatility from the entire pancreas, whereas paracrine intra-islet effects still suffice to explain coordinated pulsatile release of glucagon and somatostatin. The present review discusses how neurotransmitters contribute to the pulsatility at different levels of integration." @default.
- W2064286821 created "2016-06-24" @default.
- W2064286821 creator A5020082293 @default.
- W2064286821 creator A5055074357 @default.
- W2064286821 date "2014-09-01" @default.
- W2064286821 modified "2023-10-14" @default.
- W2064286821 title "Neurotransmitter control of islet hormone pulsatility" @default.
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- W2064286821 doi "https://doi.org/10.1111/dom.12345" @default.
- W2064286821 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25200303" @default.
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