ArticleScientific reports2021
The effects of beta-cell mass and function, intercellular coupling, and islet synchrony on [Formula: see text] dynamics.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Gap-junction-mediated bioelectric signaling required for slow muscle development and function in zebrafish.Current biology : CB · 2024Article
- Network representation of multicellular activity in pancreatic islets: Technical considerations for functional connectivity analysis.PLoS computational biology · 2024Article
- A primer on modelling pancreatic islets: from models of coupled β-cells to multicellular islet models.Islets · 2023Review
- Gap junction mediated bioelectric coordination is required for slow muscle development, organization, and function.bioRxiv : the preprint server for biology · 2023Article
- Multilevel synchronization of humanFrontiers in network physiology · 2023Article
- From Isles of Königsberg to Islets of Langerhans: Examining the Function of the Endocrine Pancreas Through Network Science.Frontiers in endocrinology · 2022Review
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
Type 2 diabetes (T2D) is a challenging metabolic disorder characterized by a substantial loss of [Formula: see text]-cell mass and alteration of [Formula: see text]-cell function in the islets of Langerhans, disrupting insulin secretion and glucose homeostasis. The mechanisms for deficiency in [Formula: see text]-cell mass and function during the hyperglycemia development and T2D pathogenesis are complex. To study the relative contribution of [Formula: see text]-cell mass to [Formula: see text]-cell function in T2D, we make use of a comprehensive electrophysiological model of human [Formula: see text]-cell clusters. We find that defect in [Formula: see text]-cell mass causes a functional decline in single [Formula: see text]-cell, impairment in intra-islet synchrony, and changes in the form of oscillatory patterns of membrane potential and intracellular [Formula: see text] concentration, which can lead to changes in insulin secretion dynamics and in insulin levels. The model demonstrates a good correspondence between suppression of synchronizing electrical activity and published experimental measurements. We then compare the role of gap junction-mediated electrical coupling with both [Formula: see text]-cell synchronization and metabolic coupling in the behavior of [Formula: see text] concentration dynamics within human islets. Our results indicate that inter-[Formula: see text]-cellular electrical coupling depicts a more important factor in shaping the physiological regulation of islet function and in human T2D. We further predict that varying the whole-cell conductance of delayed rectifier [Formula: see text] channels modifies oscillatory activity patterns of [Formula: see text]-cell population lacking intercellular coupling, which significantly affect [Formula: see text] concentration and insulin secretion.
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