The somatostatin-secreting pancreatic δ-cell in health and disease.
The somatostatin-secreting pancreatic δ-cell in health and disease.
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DOI：
10.1038/s41574-018-0020-6
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发表时间：
2018-07
期刊：
影响因子：
--
通讯作者：
Huising MO
中科院分区：
文献类型：
--
作者：
Rorsman P;Huising MO
The somatostatin-secreting δ-cells comprise ~5% of the cells of the pancreatic islets. The δ-cells have complex morphology and may, via cellular process, interact with many more islet cells than suggested by their low number. δ-cells are equipped with ATP-sensitive potassium channels (KATP channels). These channels are open at low glucose, but close in response to glucose stimulation. This results in membrane depolarisation, initiation of electrical activity, and somatostatin secretion. Glucose also stimulates somatostatin secretion by KATP channel-independent mechanisms. The Ca2+ signal initiated by electrical activity leads to further mobilization by intracellular Ca2+ stores. Factors released by neighbouring β-cells (like GABA and urocortin-3) amplify the glucose-induced effects on δ-cell electrical activity/somatostatin secretion. Somatostatin secreted from the δ-cell acts locally within the islets as a paracrine inhibitor of insulin and glucagon secretion. The effects of somatostatin are mediated by activation of somatostatin receptors that are coupled to the inhibitory G protein, which culminates in transient suppression of α- and β-cell electrical activity and exocytosis. There is evidence that somatostatin secretion is perturbed in diabetes. This may explain the loss of appropriate hypoglycaemia-induced glucagon secretion in diabetic animals, which can be mitigated by SSTR2 antagonists. Somatostatin secretion is stimulated by hypokalaemia, a well-known by-product of insulin therapy, and this effect may, via inhibition of glucagon secretion, increase the risk of hypoglycaemia in insulin-treated patients. It is proposed that somatostatin antagonists or agents that suppress somatostatin secretion should be considered as an adjunct to insulin therapy.
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影响因子：
4.8
作者：
Adriaenssens A;Lam BY;Billing L;Skeffington K;Sewing S;Reimann F;Gribble F
通讯作者：
Gribble F
影响因子：
8.1
作者：
DiGruccio MR;Mawla AM;Donaldson CJ;Noguchi GM;Vaughan J;Cowing-Zitron C;van der Meulen T;Huising MO
通讯作者：
Huising MO
DOI：
10.1113/jp274581
发表时间：
2018-01-15
期刊：
The Journal of physiology
影响因子：
--
作者：
Briant LJB;Reinbothe TM;Spiliotis I;Miranda C;Rodriguez B;Rorsman P
通讯作者：
Rorsman P
影响因子：
8.2
作者：
Caduff, A.;Lutz, H. U.;Theander, S.
通讯作者：
Theander, S.
影响因子：
8.2
作者：
de Heer, J.;Rasmussen, C.;Holst, J. J.
通讯作者：
Holst, J. J.