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Somatostatin secretion by Na+-dependent Ca2+-induced Ca2+ release in pancreatic delta-cells.

Vergari, Elisa (author)
Churchill Hospital
Denwood, Geoffrey (author)
Churchill Hospital
Salehi, Albert (author)
University of Gothenburg,Lund University,Lunds universitet,Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology,CRC, Clinical Research Centre,Medicinska fakulteten,Diabetes - öpatofysiologi,Forskargrupper vid Lunds universitet,CRC, Clinical Research Centre,Faculty of Medicine,Diabetes - Islet Patophysiology,Lund University Research Groups
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Zhang, Quan (author)
Churchill Hospital
Adam, Julie (author)
University of Oxford
Alrifaiy, Ahmed (author)
University of Gothenburg,Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi,Institute of Neuroscience and Physiology, Department of Physiology
Wernstedt Asterholm, Ingrid, 1978 (author)
University of Gothenburg,Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology
Benrick, Anna, 1979 (author)
University of Gothenburg,Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology
Chibalina, Margarita V (author)
Churchill Hospital
Eliasson, Lena (author)
Lund University,Lunds universitet,CRC, Clinical Research Centre,Medicinska fakulteten,Diabetes - öcellsexocytos,Forskargrupper vid Lunds universitet,CRC, Clinical Research Centre,Faculty of Medicine,Diabetes - Islet Cell Exocytosis,Lund University Research Groups
Guida, Claudia (author)
Churchill Hospital
Hill, Thomas G (author)
Churchill Hospital
Hamilton, Alexander (author)
Lund University,Lunds universitet,CRC, Clinical Research Centre,Medicinska fakulteten,Diabetes - molekylär metabolism,Forskargrupper vid Lunds universitet,CRC, Clinical Research Centre,Faculty of Medicine,Diabetes - Molecular Metabolism,Lund University Research Groups,Churchill Hospital
Ramracheya, Reshma (author)
Churchill Hospital
Reimann, Frank (author)
University of Cambridge
Rorsman, Nils J G (author)
Churchill Hospital
Spilliotis, Ioannis (author)
NIHR Biomedical Research Centre, Oxford,Churchill Hospital
Tarasov, Andrei I (author)
NIHR Biomedical Research Centre, Oxford,Churchill Hospital
Walker, Jonathan N (author)
Churchill Hospital,Royal Devon & Exeter Hospital
Rorsman, Patrik, 1959 (author)
University of Gothenburg,Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology,NIHR Biomedical Research Centre, Oxford,Churchill Hospital
Briant, Linford J B (author)
University of Oxford,Churchill Hospital
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 (creator_code:org_t)
2020-01-20
2020
English.
In: Nature metabolism. - : Springer Science and Business Media LLC. - 2522-5812. ; 2:1, s. 32-40
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  • Journal article (peer-reviewed)
Abstract Subject headings
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  • Pancreatic islets are complex micro-organs consisting of at least three different cell types: glucagon-secreting α-, insulin-producing β- and somatostatin-releasing δ-cells1. Somatostatin is a powerful paracrine inhibitor of insulin and glucagon secretion2. In diabetes, increased somatostatinergic signalling leads to defective counter-regulatory glucagon secretion3. This increases the risk of severe hypoglycaemia, a dangerous complication of insulin therapy4. The regulation of somatostatin secretion involves both intrinsic and paracrine mechanisms5 but their relative contributions and whether they interact remains unclear. Here we show that dapagliflozin-sensitive glucose- and insulin-dependent sodium uptake stimulates somatostatin secretion by elevating the cytoplasmic Na+ concentration ([Na+]i) and promoting intracellular Ca2+-induced Ca2+ release (CICR). This mechanism also becomes activated when [Na+]i is elevated following the inhibition of the plasmalemmal Na+-K+ pump by reductions of the extracellular K+ concentration emulating those produced by exogenous insulin in vivo6. Islets from some donors with type-2 diabetes hypersecrete somatostatin, leading to suppression of glucagon secretion that can be alleviated by a somatostatin receptor antagonist. Our data highlight the role of Na+ as an intracellular second messenger, illustrate the significance of the intraislet paracrine network and provide a mechanistic framework for pharmacological correction of the hormone secretion defects associated with diabetes that selectively target the δ-cells.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Fysiologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Physiology (hsv//eng)
MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Endokrinologi och diabetes (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Endocrinology and Diabetes (hsv//eng)

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