ArticleAmerican journal of physiology. Endocrinology and metabolism2013
Slow oscillations of KATP conductance in mouse pancreatic islets provide support for electrical bursting driven by metabolic oscillations.
Article in American journal of physiology. Endocrinology and metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 37 citations in OpenAlex.
- Deconstructing the integrated oscillator model for pancreatic β-cells.Mathematical biosciences · 2023Article
- Similarities in Calcium Oscillations Between Neonatal Mouse Islets and Mature Islets Exposed to Chronic Hyperglycemia.Endocrinology · 2022Article
- Oscillations in K(ATP) conductance drive slow calcium oscillations in pancreatic β-cells.Biophysical journal · 2022Article
- Beta-Cell Ion Channels and Their Role in Regulating Insulin Secretion.Comprehensive Physiology · 2021Review
- Observing Islet Function and Islet-Immune Cell Interactions in Live Pancreatic Tissue Slices.Journal of visualized experiments : JoVE · 2021Article
- CDK2 limits the highly energetic secretory program of mature β cells by restricting PEP cycle-dependent KCell reports · 2021Article
- ER stress increases store-operated CaThe Journal of biological chemistry · 2020Article
- Reducing Glucokinase Activity Restores Endogenous Pulsatility and Enhances Insulin Secretion in Islets From db/db Mice.Endocrinology · 2018Article
- Closing in on the Mechanisms of Pulsatile Insulin Secretion.Diabetes · 2018Article
- Spatially Organized β-Cell Subpopulations Control Electrical Dynamics across Islets of Langerhans.Biophysical journal · 2017Article
- Upregulation of an inward rectifying K+ channel can rescue slow Ca2+ oscillations in K(ATP) channel deficient pancreatic islets.PLoS computational biology · 2017Article
- Stromal Interaction Molecule 1 (STIM1) Regulates ATP-sensitive Potassium (The Journal of biological chemistry · 2017Article
- Osteopontin activates the diabetes-associated potassium channel TALK-1 in pancreatic β-cells.PloS one · 2017Article
- Pancreatic β-Cells From Mice Offset Age-Associated Mitochondrial Deficiency With Reduced KATP Channel Activity.Diabetes · 2016Article
- Ca2+ Effects on ATP Production and Consumption Have Regulatory Roles on Oscillatory Islet Activity.Biophysical journal · 2016Article
- Chronic Glucose Exposure Systematically Shifts the Oscillatory Threshold of Mouse Islets: Experimental Evidence for an Early Intrinsic Mechanism of Compensation for Hyperglycemia.Endocrinology · 2016Article
- Article
- Modeling of glucose-induced cAMP oscillations in pancreatic β cells: cAMP rocks when metabolism rolls.Biophysical journal · 2015Article
- TASK-1 Potassium Channels Limit Pancreatic α-Cell Calcium Influx and Glucagon Secretion.Molecular endocrinology (Baltimore, Md.) · 2015Article
- Pulsatile insulin secretion, impaired glucose tolerance and type 2 diabetes.Molecular aspects of medicine · 2015Review
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
We used the patch clamp technique in situ to test the hypothesis that slow oscillations in metabolism mediate slow electrical oscillations in mouse pancreatic islets by causing oscillations in KATP channel activity. Total conductance was measured over the course of slow bursting oscillations in surface β-cells of islets exposed to 11.1 mM glucose by either switching from current clamp to voltage clamp at different phases of the bursting cycle or by clamping the cells to -60 mV and running two-second voltage ramps from -120 to -50 mV every 20 s. The membrane conductance, calculated from the slopes of the ramp current-voltage curves, oscillated and was larger during the silent phase than during the active phase of the burst. The ramp conductance was sensitive to diazoxide, and the oscillatory component was reduced by sulfonylureas or by lowering extracellular glucose to 2.8 mM, suggesting that the oscillatory total conductance is due to oscillatory KATP channel conductance. We demonstrate that these results are consistent with the Dual Oscillator model, in which glycolytic oscillations drive slow electrical bursting, but not with other models in which metabolic oscillations are secondary to calcium oscillations. The simulations also confirm that oscillations in membrane conductance can be well estimated from measurements of slope conductance and distinguished from gap junction conductance. Furthermore, the oscillatory conductance was blocked by tolbutamide in isolated β-cells. The data, combined with insights from mathematical models, support a mechanism of slow (∼5 min) bursting driven by oscillations in metabolism, rather than by oscillations in the intracellular free calcium concentration.
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