ArticleEndocrinology2016
Chronic Glucose Exposure Systematically Shifts the Oscillatory Threshold of Mouse Islets: Experimental Evidence for an Early Intrinsic Mechanism of Compensation for Hyperglycemia.
Article in Endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 38 citations in OpenAlex.
- Article
- Article
- A mathematical model for ketosis-prone diabetes suggests the existence of multiple pancreatic β-cell inactivation mechanisms.bioRxiv : the preprint server for biology · 2025Article
- One-hour glucose is an earlier marker of dysglycemia than two-hour glucose.Diabetes research and clinical practice · 2023Article
- CaAmerican journal of physiology. Endocrinology and metabolism · 2023Review
- Glucokinase Inhibition: A Novel Treatment for Diabetes?Diabetes · 2023Review
- Similarities in Calcium Oscillations Between Neonatal Mouse Islets and Mature Islets Exposed to Chronic Hyperglycemia.Endocrinology · 2022Article
- Beta-Cell Ion Channels and Their Role in Regulating Insulin Secretion.Comprehensive Physiology · 2021Review
- Chronically Elevated Exogenous Glucose Elicits Antipodal Effects on the Proteome Signature of Differentiating Human iPSC-Derived Pancreatic Progenitors.International journal of molecular sciences · 2021Article
- Postnatal maturation of calcium signaling in islets of Langerhans from neonatal mice.Cell calcium · 2021Article
- Essential requirement of complex number for oscillatory phenomenon in intracellular trafficking process.Computational and structural biotechnology journal · 2021Article
- Preferential Gq signaling in diabetes: an electrical switch in incretin action and in diabetes progression?The Journal of clinical investigation · 2020Article
- Type 2 diabetes: one disease, many pathways.American journal of physiology. Endocrinology and metabolism · 2020Article
- ER stress increases store-operated CaThe Journal of biological chemistry · 2020Article
- Chronic stimulation induces adaptive potassium channel activity that restores calcium oscillations in pancreatic islets in vitro.American journal of physiology. Endocrinology and metabolism · 2020Article
- Reducing Glucokinase Activity to Enhance Insulin Secretion: A Counterintuitive Theory to Preserve Cellular Function and Glucose Homeostasis.Frontiers in endocrinology · 2020Article
- The role of membrane excitability in pancreatic β-cell glucotoxicity.Scientific reports · 2019Article
- Reducing Glucokinase Activity Restores Endogenous Pulsatility and Enhances Insulin Secretion in Islets From db/db Mice.Endocrinology · 2018Article
- Automated microfluidic droplet sampling with integrated, mix-and-read immunoassays to resolve endocrine tissue secretion dynamics.Lab on a chip · 2018Article
- Short-term high glucose culture potentiates pancreatic beta cell function.Scientific reports · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Mouse islets exhibit glucose-dependent oscillations in electrical activity, intracellular Ca(2+) and insulin secretion. We developed a mathematical model in which a left shift in glucose threshold helps compensate for insulin resistance. To test this experimentally, we exposed isolated mouse islets to varying glucose concentrations overnight and monitored their glucose sensitivity the next day by measuring intracellular Ca(2+), electrical activity, and insulin secretion. Glucose sensitivity of all oscillation modes was increased when overnight glucose was greater than 2.8mM. To determine whether threshold shifts were a direct effect of glucose or involved secreted insulin, the KATP opener diazoxide (Dz) was coapplied with glucose to inhibit insulin secretion. The addition of Dz or the insulin receptor antagonist s961 increased islet glucose sensitivity, whereas the KATP blocker tolbutamide tended to reduce it. This suggests insulin and glucose have opposing actions on the islet glucose threshold. To test the hypothesis that the threshold shifts were due to changes in plasma membrane KATP channels, we measured cell KATP conductance, which was confirmed to be reduced by high glucose pretreatment and further reduced by Dz. Finally, treatment of INS-1 cells with glucose and Dz overnight reduced high affinity sulfonylurea receptor (SUR1) trafficking to the plasma membrane vs glucose alone, consistent with insulin increasing KATP conductance by altering channel number. The results support a role for metabolically regulated KATP channels in the maintenance of glucose homeostasis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.