scholarly journals Tetraspanin‐7 regulation of L‐type voltage‐dependent calcium channels controls pancreatic β‐cell insulin secretion

2020 ◽  
Vol 598 (21) ◽  
pp. 4887-4905 ◽  
Author(s):  
Matthew T. Dickerson ◽  
Prasanna K. Dadi ◽  
Regan B. Butterworth ◽  
Arya Y. Nakhe ◽  
Sarah M. Graff ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Calcium Channels ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels ◽  
Tetraspanin 7

Resveratrol-induced inhibition of insulin secretion from rat pancreatic islets: evidence for pivotal role of metabolic disturbances

2007 ◽  
Vol 293 (4) ◽  
pp. E901-E907 ◽  
Author(s):  
Tomasz Szkudelski
Keyword(s):  
Insulin Secretion ◽  
Protein Kinase ◽  
Calcium Channels ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Estrogenic Activity ◽  
Hormone Secretion ◽  
Lactate Production ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels

Resveratrol is a stilbene present in different plant species and exerting numerous beneficial effects, including prevention of diabetes and attenuation of some diabetic complications. Its inhibitory effect on insulin secretion was recently documented, but the exact mechanism underlying this action remains unknown. Experiments employing diazoxide and a high concentration of K+revealed that, in depolarized pancreatic islets incubated for 90 min with resveratrol (1, 10, and 100 μM), insulin secretion stimulated by glucose and leucine was impaired. The attenuation of the insulin secretory response to 6.7 mM glucose was not abrogated by blockade of intracellular estrogen receptors and was found to be accompanied by diminished islet glucose oxidation, enhanced lactate production, and reduced ATP levels. Glucose-induced hyperpolarization of the mitochondrial membrane was also reduced in the presence of resveratrol. Moreover, in depolarized islets incubated with 2.8 mM glucose, activation of protein kinase C or protein kinase A potentiated insulin release; however, under these conditions, resveratrol was ineffective. Further studies also revealed that, under conditions of blocked voltage-dependent calcium channels, the stilbene reduced insulin secretion induced by a combination of glucose with forskolin. These data demonstrate that resveratrol 1) inhibits the amplifying pathway of insulin secretion, 2) exerts an insulin-suppressive effect independently of its estrogenic/anti-estrogenic activity, 3) shifts islet glucose metabolism from mitochondrial oxidation to anaerobic, 4) fails to abrogate insulin release promoted without metabolic events, and 5) does not suppress hormone secretion as a result of the direct inhibition of Ca2+influx through voltage-dependent calcium channels.

scholarly journals Cyanidin Stimulates Insulin Secretion and Pancreatic β-Cell Gene Expression through Activation of l-type Voltage-Dependent Ca2+ Channels

Nutrients ◽  
2017 ◽  
Vol 9 (8) ◽  
pp. 814 ◽  
Author(s):  
Tanyawan Suantawee ◽  
Sara Elazab ◽  
Walter Hsu ◽  
Shaomian Yao ◽  
Henrique Cheng ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Secretion ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Voltage Dependent ◽  
Cell Gene Expression ◽  
Cell Gene ◽  
Ca2 Channels

scholarly journals Ontology of the apelinergic system in mouse pancreas during pregnancy and relationship with β-cell mass

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Brenda Strutt ◽  
Sandra Szlapinski ◽  
Thineesha Gnaneswaran ◽  
Sarah Donegan ◽  
Jessica Hill ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Insulin Secretion ◽  
Glucose Transporter ◽  
Cell Mass ◽  
Elevated Serum ◽  
Pancreatic Β Cell ◽  
Β Cells ◽  
Β Cell ◽  
Glucose Transporter 2 ◽  
Glucose Stimulated Insulin Secretion

AbstractThe apelin receptor (Aplnr) and its ligands, Apelin and Apela, contribute to metabolic control. The insulin resistance associated with pregnancy is accommodated by an expansion of pancreatic β-cell mass (BCM) and increased insulin secretion, involving the proliferation of insulin-expressing, glucose transporter 2-low (Ins+Glut2LO) progenitor cells. We examined changes in the apelinergic system during normal mouse pregnancy and in pregnancies complicated by glucose intolerance with reduced BCM. Expression of Aplnr, Apelin and Apela was quantified in Ins+Glut2LO cells isolated from mouse pancreata and found to be significantly higher than in mature β-cells by DNA microarray and qPCR. Apelin was localized to most β-cells by immunohistochemistry although Aplnr was predominantly associated with Ins+Glut2LO cells. Aplnr-staining cells increased three- to four-fold during pregnancy being maximal at gestational days (GD) 9–12 but were significantly reduced in glucose intolerant mice. Apelin-13 increased β-cell proliferation in isolated mouse islets and INS1E cells, but not glucose-stimulated insulin secretion. Glucose intolerant pregnant mice had significantly elevated serum Apelin levels at GD 9 associated with an increased presence of placental IL-6. Placental expression of the apelinergic axis remained unaltered, however. Results show that the apelinergic system is highly expressed in pancreatic β-cell progenitors and may contribute to β-cell proliferation in pregnancy.

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