The Sherman-Rinzel-Keizer Model for Bursting Electrical Activity in the Pancreatic β-Cell

1991 ◽  
pp. 34-53 ◽  
Author(s):  
Mark Pernarowski ◽  
Robert M. Miura ◽  
J. Kevorkian
Keyword(s):  
Electrical Activity ◽  
Pancreatic Β Cell ◽  
Β Cell

scholarly journals Mathematical models of electrical activity of the pancreatic β-cell: A physiological review

Islets ◽  
2014 ◽  
Vol 6 (3) ◽  
pp. e949195 ◽  
Author(s):  
Gerardo J Félix-Martínez ◽  
J Rafael Godínez-Fernández
Keyword(s):  
Electrical Activity ◽  
Mathematical Models ◽  
Pancreatic Β Cell ◽  
Β Cell

scholarly journals Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men

2018 ◽  
Vol 98 (1) ◽  
pp. 117-214 ◽  
Author(s):  
Patrik Rorsman ◽  
Frances M. Ashcroft
Keyword(s):  
Insulin Secretion ◽  
Electrical Activity ◽  
Glucose Concentration ◽  
Glucose Sensor ◽  
Blood Glucose Concentration ◽  
Secretory Granules ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Chronic Hyperglycemia ◽  
Cell Transcriptome

The pancreatic β-cell plays a key role in glucose homeostasis by secreting insulin, the only hormone capable of lowering the blood glucose concentration. Impaired insulin secretion results in the chronic hyperglycemia that characterizes type 2 diabetes (T2DM), which currently afflicts >450 million people worldwide. The healthy β-cell acts as a glucose sensor matching its output to the circulating glucose concentration. It does so via metabolically induced changes in electrical activity, which culminate in an increase in the cytoplasmic Ca2+ concentration and initiation of Ca2+-dependent exocytosis of insulin-containing secretory granules. Here, we review recent advances in our understanding of the β-cell transcriptome, electrical activity, and insulin exocytosis. We highlight salient differences between mouse and human β-cells, provide models of how the different ion channels contribute to their electrical activity and insulin secretion, and conclude by discussing how these processes become perturbed in T2DM.

Regulation of pancreatic β-cell electrical activity and insulin release by physiological amino acid concentrations

1997 ◽  
Vol 433 (6) ◽  
pp. 699-704 ◽  
Author(s):  
Sonia Bolea ◽  
Jose A. G. Pertusa ◽  
Franz Martín ◽  
Juan V. Sanchez-Andrés ◽  
B. Soria
Keyword(s):  
Amino Acid ◽  
Electrical Activity ◽  
Insulin Release ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Amino Acid Concentrations

scholarly journals Molecular mechanisms responsible for the sexual dimorphism in pancreatic β-cell insulin release

2021 ◽  
Vol 154 (9) ◽  
Author(s):  
Noelia Jacobo-Piqueras ◽  
Tamara Theiner ◽  
Stefanie M. Geisler ◽  
Petronel Tuluc
Keyword(s):  
Sexual Dimorphism ◽  
Electrical Activity ◽  
Insulin Release ◽  
Molecular Mechanisms ◽  
Resting Membrane Potential ◽  
Pancreatic Β Cell ◽  
Β Cells ◽  
Β Cell ◽  
Specific Expression ◽  
Extracellular Glucose Concentration

In humans, type 2 diabetes mellitus (T2DM) has a higher incidence in males compared to females, a phenotype recapitulated by many rodent models. While the sex difference in insulin sensitivity partially accounts for this phenomenon, hitherto uncharacterized differences in pancreatic β-cell insulin release strongly contribute. Here, we show that stepwise increase in extracellular glucose concentration (2, 5, 7.5, 10, 15, 20 mM) induced electrical activity in β cells of both sexes with similar glucose sensitivity (female, EC50 = 9.45 ± 0.15 mM; male, EC50 = 9.42 ± 0.16 mM). However, female β cells’ resting membrane potential (RMP) and inter-spike potential (IP) were significantly higher compared to males (e.g., at 15 mM glucose: male RMP = −82.7 ± 6.3, IP = −74.3 ± 6.8 mV; female RMP = −50.0 ± 7.1, IP = −41.2 ± 7.3 mV). Females also showed higher frequency of trains of action potential (AP; at 10 mM glucose: male F = 1.13 ± 0.15 trains/min; female F = 1.78 ± 0.25 trains/min) and longer AP-burst duration (e.g., at 10 mM glucose: male, 241 ± 30.8 ms; female, 419 ± 60.2 ms). The higher RMP in females reduced the voltage-gated calcium channel (CaV) availability by ∼60%. This explains the paradoxical observation that, despite identical CaV expression levels and higher electrical activity, the islet Ca2+ transients were smaller in females compared to males. Interestingly, the different RMPs are not caused by altered KATP, TASK, or TALK K+ currents. However, stromatoxin-1–sensitive KV2.1 K+ current amplitude was almost double in males (IK = 130.93 ± 7.05 pA/pF) compared to females (IK = 75.85 ± 11.3 pA/pF) when measured at +80 mV. Our results are in agreement with previous findings showing that KV2.1 genetic deletion or pharmacological block leads to higher insulin release and β-cell survival. Therefore, we propose the sex-specific expression of KV2.1 to be the mechanism underlying the observed sexual dimorphism in insulin release and the incidence of T2DM.

EFFECTS OF ADRENALINE AND NORADRENALINE ON GLUCOSE-INDUCED ELECTRICAL ACTIVITY OF MOUSE PANCREATIC β CELL

1983 ◽  
Vol 68 (2) ◽  
pp. 247-258 ◽  
Author(s):  
Sonia Santana De Sa ◽  
Rosa Ferrer ◽  
Eduardo Rojas ◽  
Illani Atwater
Keyword(s):  
Electrical Activity ◽  
Pancreatic Β Cell ◽  
Β Cell

Adipokines as key players in β cell function and failure

2019 ◽  
Vol 133 (22) ◽  
pp. 2317-2327 ◽  
Author(s):  
Nicolás Gómez-Banoy ◽  
James C. Lo
Keyword(s):  
Metabolic Diseases ◽  
Cell Function ◽  
Whole Body ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Axis ◽  
Β Cell Function ◽  
Prevalence Of Obesity ◽  
Specific Factors ◽  
Whole Body Metabolism

Abstract The growing prevalence of obesity and its related metabolic diseases, mainly Type 2 diabetes (T2D), has increased the interest in adipose tissue (AT) and its role as a principal metabolic orchestrator. Two decades of research have now shown that ATs act as an endocrine organ, secreting soluble factors termed adipocytokines or adipokines. These adipokines play crucial roles in whole-body metabolism with different mechanisms of action largely dependent on the tissue or cell type they are acting on. The pancreatic β cell, a key regulator of glucose metabolism due to its ability to produce and secrete insulin, has been identified as a target for several adipokines. This review will focus on how adipokines affect pancreatic β cell function and their impact on pancreatic β cell survival in disease contexts such as diabetes. Initially, the “classic” adipokines will be discussed, followed by novel secreted adipocyte-specific factors that show therapeutic promise in regulating the adipose–pancreatic β cell axis.

INCRETIN AND DIABETES

2011 ◽  
pp. 5-10
Author(s):  
Huu Dang Tran
Keyword(s):  
Type 2 Diabetes ◽  
Cell Proliferation ◽  
Glycaemic Control ◽  
Animal Studies ◽  
Dipeptidyl Peptidase ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Glucose Sensitivity ◽  
Cell Glucose

The incretins are peptide hormones secreted from the gut in response to food. They increase the secretion of insulin. The incretin response is reduced in patients with type 2 diabetes so drugs acting on incretins may improve glycaemic control. Incretins are metabolised by dipeptidyl peptidase, so selectively inhibiting this enzyme increases the concentration of circulating incretins. A similar effect results from giving an incretin analogue that cannot be cleaved by dipeptidyl peptidase. Studies have identified other actions including improvement in pancreatic β cell glucose sensitivity and, in animal studies, promotion of pancreatic β cell proliferation and reduction in β cell apoptosis.

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