scholarly journals Src regulates insulin secretion and glucose metabolism by influencing subcellular localization of glucokinase in pancreatic β‐cells

2015 ◽  
Vol 7 (2) ◽  
pp. 171-178 ◽  
Author(s):  
Hiroki Sato ◽  
Kazuaki Nagashima ◽  
Masahito Ogura ◽  
Yuichi Sato ◽  
Yumiko Tahara ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Glucose Metabolism ◽  
Subcellular Localization ◽  
Β Cells ◽  
Pancreatic Β Cells

scholarly journals Somatostatin Inhibits Oxidative Respiration in Pancreatic β-Cells

Endocrinology ◽  
2006 ◽  
Vol 147 (3) ◽  
pp. 1527-1535 ◽  
Author(s):  
Mathew Daunt ◽  
Oliver Dale ◽  
Paul A. Smith
Keyword(s):  
Insulin Secretion ◽  
Glucose Metabolism ◽  
Somatostatin Receptor ◽  
Katp Channels ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
K Channels ◽  
Min6 Cells ◽  
Voltage Gated ◽  
Mouse Islets

Somatostatin potently inhibits insulin secretion from pancreatic β-cells. It does so via activation of ATP-sensitive K+-channels (KATP) and G protein-regulated inwardly rectifying K+-channels, which act to decrease voltage-gated Ca2+-influx, a process central to exocytosis. Because KATP channels, and indeed insulin secretion, is controlled by glucose oxidation, we investigated whether somatostatin inhibits insulin secretion by direct effects on glucose metabolism. Oxidative metabolism in β-cells was monitored by measuring changes in the O2 consumption (ΔO2) of isolated mouse islets and MIN6 cells, a murine-derived β-cell line. In both models, glucose-stimulated ΔO2, an effect closely associated with inhibition of KATP channel activity and induction of electrical activity (r > 0.98). At 100 nm, somatostatin abolished glucose-stimulated ΔO2 in mouse islets (n = 5, P < 0.05) and inhibited it by 80 ± 28% (n = 17, P < 0.01) in MIN6 cells. Removal of extracellular Ca2+, 5 mm Co2+, or 20 μm nifedipine, conditions that inhibit voltage-gated Ca2+ influx, did not mimic but either blocked or reduced the effect of the peptide on ΔO2. The nutrient secretagogues, methylpyruvate (10 mm) and α-ketoisocaproate (20 mm), also stimulated ΔO2, but this was unaffected by somatostatin. Somatostatin also reversed glucose-induced hyperpolarization of the mitochondrial membrane potential monitored using rhodamine-123. Application of somatostatin receptor selective agonists demonstrated that the peptide worked through activation of the type 5 somatostatin receptor. In conclusion, somatostatin inhibits glucose metabolism in murine β-cells by an unidentified Ca2+-dependent mechanism. This represents a new signaling pathway by which somatostatin can inhibit cellular functions regulated by glucose metabolism.

scholarly journals Somatostatin analogues for the treatment of hyperinsulinaemic hypoglycaemia

2020 ◽  
Vol 11 ◽  
pp. 204201882096506
Author(s):  
Basma Haris ◽  
Saras Saraswathi ◽  
Khalid Hussain
Keyword(s):  
Insulin Secretion ◽  
Blood Glucose ◽  
Glucose Metabolism ◽  
Therapeutic Effect ◽  
Glucagon Secretion ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Hyperinsulinaemic Hypoglycaemia ◽  
Glucose Levels ◽  
Blood Glucose Levels

Hyperinsulinaemic hypoglycaemia (HH) is a biochemical finding of low blood glucose levels due to the dysregulation of insulin secretion from pancreatic β-cells. Under normal physiological conditions, glucose metabolism is coupled to β-cell insulin secretion so that blood glucose levels are maintained within the physiological range of 3.5–5.5 mmol/L. However, in HH this coupling of glucose metabolism to insulin secretion is perturbed so that insulin secretion becomes unregulated. HH typically occurs in the neonatal, infancy and childhood periods and can be due to many different causes. Adults can also present with HH but the causes in adults tend to be different. Somatostatin (SST) is a peptide hormone that is released by the delta cells (δ-cells) in the pancreas. It binds to G protein-coupled SST receptors to regulate a variety of location-specific and selective functions such as hormone inhibition, neurotransmission and cell proliferation. SST plays a potent role in the regulation of both insulin and glucagon secretion in response to changes in glucose levels by negative feedback mechanism. The half-life of SST is only 1–3 min due to quick degradation by peptidases in plasma and tissues. Thus, a direct continuous intravenous or subcutaneous infusion is required to achieve the therapeutic effect. These limitations prompted the discovery of SST analogues such as octreotide and lanreotide, which have longer half-lives and therefore can be administered as injections. SST analogues are used to treat different forms of HH in children and adults and therapeutic effect is achieved by suppressing insulin secretion from pancreatic β-cells by complex mechanisms. These treatments are associated with several side effects, especially in the newborn period, with necrotizing enterocolitis being the most serious side effect and hence SS analogues should be used with extreme caution in this age group.

scholarly journals Glycated albumin suppresses glucose-induced insulin secretion by impairing glucose metabolism in rat pancreatic β-cells

2011 ◽  
Vol 8 (1) ◽  
pp. 20 ◽  
Author(s):  
Takayuki Shiraki ◽  
Yoshikazu Miura ◽  
Tokihiko Sawada ◽  
Toshie Okada ◽  
Yuhki Sakuraoka ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Glucose Metabolism ◽  
Glycated Albumin ◽  
Β Cells ◽  
Pancreatic Β Cells

Congenital hyperinsulinism due to compound heterozygous mutations in ABCC8 responsive to diazoxide therapy

2020 ◽  
Vol 33 (5) ◽  
pp. 671-674
Author(s):  
Tashunka Taylor-Miller ◽  
Jayne Houghton ◽  
Paul Munyard ◽  
Yadlapalli Kumar ◽  
Clinda Puvirajasinghe ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Compound Heterozygous ◽  
Congenital Hyperinsulinism ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Newborn Period ◽  
Case Presentation ◽  
Male Baby ◽  
Common Causes ◽  
Compound Heterozygous Mutations

AbstractBackgroundCongenital hyperinsulinism (CHI), a condition characterized by dysregulation of insulin secretion from the pancreatic β cells, remains one of the most common causes of hyperinsulinemic, hypoketotic hypoglycemia in the newborn period. Mutations in ABCC8 and KCNJ11 constitute the majority of genetic forms of CHI.Case presentationA term macrosomic male baby, birth weight 4.81 kg, born to non-consanguineous parents, presented on day 1 of life with severe and persistent hypoglycemia. The biochemical investigations confirmed a diagnosis of CHI. Diazoxide was started and progressively increased to 15 mg/kg/day to maintain normoglycemia. Sequence analysis identified compound heterozygous mutations in ABCC8 c.4076C>T and c.4119+1G>A inherited from the unaffected father and mother, respectively. The mutations are reported pathogenic. The patient is currently 7 months old with a sustained response to diazoxide.ConclusionsBiallelic ABCC8 mutations are known to result in severe, diffuse, diazoxide-unresponsive hypoglycemia. We report a rare patient with CHI due to compound heterozygous mutations in ABCC8 responsive to diazoxide.

scholarly journals Author Correction: CD44 variant inhibits insulin secretion in pancreatic β cells by attenuating LAT1-mediated amino acid uptake

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Nana Kobayashi ◽  
Shogo Okazaki ◽  
Oltea Sampetrean ◽  
Junichiro Irie ◽  
Hiroshi Itoh ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Amino Acid ◽  
Amino Acid Uptake ◽  
Acid Uptake ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Cd44 Variant

scholarly journals D2-Like Receptors Mediate Dopamine-Inhibited Insulin Secretion via Ion Channels in Rat Pancreatic β-Cells

2020 ◽  
Vol 11 ◽  
Author(s):  
Mengmeng Liu ◽  
Lele Ren ◽  
Xiangqin Zhong ◽  
Yaqin Ding ◽  
Tao Liu ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Ion Channels ◽  
Β Cells ◽  
Pancreatic Β Cells

Jiawei Erzhiwan improves menopausal metabolic syndrome by enhancing insulin secretion in pancreatic β cells

2016 ◽  
Vol 14 (11) ◽  
pp. 823-834 ◽  
Author(s):  
Xiao-Meng WAN ◽  
Mu ZHANG ◽  
Pei ZHANG ◽  
Zhi-Shen XIE ◽  
Feng-Guo XU ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Insulin Secretion ◽  
Β Cells ◽  
Pancreatic Β Cells

scholarly journals Brain-selective Kinase 2 (BRSK2) Phosphorylation on PCTAIRE1 Negatively Regulates Glucose-stimulated Insulin Secretion in Pancreatic β-Cells

2012 ◽  
Vol 287 (36) ◽  
pp. 30368-30375 ◽  
Author(s):  
Xin-Ya Chen ◽  
Xiu-Ting Gu ◽  
Hexige Saiyin ◽  
Bo Wan ◽  
Yu-Jing Zhang ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Glucose Stimulated Insulin Secretion

scholarly journals Regulation of voltage-gated K+channels by glucose metabolism in pancreatic β-cells

FEBS Letters ◽  
2009 ◽  
Vol 583 (13) ◽  
pp. 2225-2230 ◽  
Author(s):  
Masashi Yoshida ◽  
Katsuya Dezaki ◽  
Shiho Yamato ◽  
Atsushi Aoki ◽  
Hitoshi Sugawara ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
K Channels ◽  
Voltage Gated
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