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A selective nonpeptide somatostatin receptor 5 agonist effectively decreases insulin secretion in hyperinsulinism.
J Biol Chem
June 2023
Division of Endocrinology and Diabetes, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA; Department of Pediatrics, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA. Electronic address:
Congenital hyperinsulinism (HI), a beta cell disorder most commonly caused by inactivating mutations of beta cell K channels, results in dysregulated insulin secretion and persistent hypoglycemia. Children with K-HI are unresponsive to diazoxide, the only FDA-approved drug for HI, and utility of octreotide, the second-line therapy, is limited because of poor efficacy, desensitization, and somatostatin receptor type 2 (SST2)-mediated side effects. Selective targeting of SST5, an SST receptor associated with potent insulin secretion suppression, presents a new avenue for HI therapy.
View Article and Find Full Text PDFGlucose inhibits glucagon secretion by decreasing [Ca] and by reducing the efficacy of Ca on exocytosis via somatostatin-dependent and independent mechanisms.
Mol Metab
July 2022
Université Catholique de Louvain, Institut de Recherche Expérimentale et Clinique, Pôle d'Endocrinologie, Diabète et Nutrition, Brussels, Belgium. Electronic address:
Objective: The mechanisms by which glucose stimulates insulin secretion from β-cells are well established and involve inhibition of ATP-sensitive K (K) channels, followed by a rise in [Ca] that triggers exocytosis. However, the mechanisms by which glucose controls glucagon release from α-cells are much less known. In particular, it is debated whether the sugar controls glucagon secretion by changing α-cell [Ca], and whether K channels or paracrine factors are involved.
View Article and Find Full Text PDFK channel blockers control glucagon secretion by distinct mechanisms: A direct stimulation of α-cells involving a [Ca] rise and an indirect inhibition mediated by somatostatin.
Mol Metab
November 2021
Université Catholique de Louvain, Institut de Recherche Expérimentale et Clinique, Pôle d'Endocrinologie, Diabète et Nutrition, Brussels, Belgium. Electronic address:
Objective: Glucagon is secreted by pancreatic α-cells in response to hypoglycemia and its hyperglycemic effect helps to restore normal blood glucose. Insulin and somatostatin (SST) secretions from β- and δ-cells, respectively, are stimulated by glucose by mechanisms involving an inhibition of their ATP-sensitive K (K) channels, leading to an increase in [Ca] that triggers exocytosis. Drugs that close K channels, such as sulfonylureas, are used to stimulate insulin release in type 2 diabetic patients.
View Article and Find Full Text PDFSomatostatin promotes glucose generation of Caoscillations in pancreatic islets both in the absence and presence of tolbutamide.
Cell Calcium
September 2018
Department of Medical Cell Biology, Uppsala University, Biomedicum Box 571, SE-75123 Uppsala, Sweden.
Many cellular processes, including pulsatile release of insulin, are triggered by increase of cytoplasmic Ca. This study examines how somatostatin affects glucose generation of cytoplasmic Ca oscillations in mouse islets in absence and presence of tolbutamide blockade of the K channels. Ca was measured with dual wavelength microflurometry in isolated islets loaded with the indicator Fura-2.
View Article and Find Full Text PDFN-(2-methoxyphenyl) benzenesulfonamide, a novel regulator of neuronal G protein-gated inward rectifier K channels.
Eur J Pharmacol
November 2017
Department of Pharmacology, Physiology & Neuroscience, University of South Carolina, School of Medicine, Columbia, SC, United States.
G protein-gated inward rectifier K (GIRK) channels are members of the super-family of proteins known as inward rectifier K (Kir) channels and are expressed throughout the peripheral and central nervous systems. Neuronal GIRK channels are the downstream targets of a number of neuromodulators including opioids, somatostatin, dopamine and cannabinoids. Previous studies have demonstrated that the ATP-sensitive K channel, another member of the Kir channel family, is regulated by sulfonamide drugs.
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