ArticleBiophysical journal2009
Accounting for near-normal glucose sensitivity in Kir6.2[AAA] transgenic mice.
Article in Biophysical journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Intrinsic islet heterogeneity and gap junction coupling determine spatiotemporal Ca²⁺ wave dynamics.Biophysical journal · 2014Article
- Modeling K,ATP--dependent excitability in pancreatic islets.Biophysical journal · 2014Article
- Cellular communication and heterogeneity in pancreatic islet insulin secretion dynamics.Trends in endocrinology and metabolism: TEM · 2014Review
- Dimensionality and size scaling of coordinated Ca(2+) dynamics in MIN6 β-cell clusters.Biophysical journal · 2014Article
- Article
- Calcium and Metabolic Oscillations in Pancreatic Islets: Who's Driving the Bus?SIAM journal on applied dynamical systemsArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
K(ir)6.2[AAA] transgenic mouse islets exhibit mosaicism such that approximately 70% of the beta-cells have nonfunctional ATP-sensitive potassium (K(ATP)) channels, whereas the remainder have normal K(ATP) function. Despite this drastic reduction, the glucose dose-response curve is only shifted by approximately 2 mM. We use a previously published mathematical model, in which K(ATP) conductance is increased by rises in cytosolic calcium through indirect effects on metabolism, to investigate how cells could compensate for the loss of K(ATP) conductance. Compensation is favored by the assumption that only a small fraction of K(ATP) channels are open during oscillations, which renders it easy to upregulate the open fraction via a modest elevation of calcium. We show further that strong gap-junctional coupling of both membrane potential and calcium is needed to overcome the stark heterogeneity of cell properties in these mosaic islets.
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Registered trials
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