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Articles by Anne Gresch
Publisher Correction: Exploring pancreatic beta-cell subgroups and their connectivity - Nature Metabolism
Correction to: Nature Metabolism https://doi.org/10.1038/s42255-024-01097-6, published online 8 August 2024. This paper was originally published as an Article under a Creative Commons Attribution 4.0 International license, © The Author(s), whereas it should have been published as a Review Article under standard Springer Nature license (© The Author(s), under exclusive licence to Springer Nature Limited), as is now amended in the HTML and PDF versions of the article.
Exploring pancreatic beta-cell subgroups and their connectivity - Nature Metabolism
Abstract Functional pancreatic islet beta cells are essential to ensure glucose homeostasis across species from zebrafish to humans. These cells show significant heterogeneity, and emerging studies have revealed that connectivity across a hierarchical network is required for normal insulin release. Here, we discuss current thinking and areas of debate around intra-islet connectivity, cellular hierarchies and potential “controlling” beta-cell populations.
Beta-cell intrinsic dynamics rather than gap junction structure dictates subpopulations in the islet functional network
Accepted manuscript, PDF only. Full online edition to follow. Author Accepted Manuscript PDF only version. The full online version will follow soon. Accepted Manuscript published November 29, 2023 (This version) Accepted November 27, 2023 Received August 31, 2022 Share this article Cite this article Beta-cell intrinsic dynamics rather than gap junction structure dictates subpopulations in the islet functional network eLife 12:e83147.
Resolving spatiotemporal electrical signaling within the islet via CMOS microelectrode arrays
Abstract Glucose-stimulated beta-cells synchronize calcium waves across the islet to recruit more beta-cells for insulin secretion. Compared to calcium dynamics, the formation and cell-to-cell propagation of electrical signals within the islet are poorly characterized.
TGR5 Activation Promotes Stimulus-Secretion Coupling of Pancreatic β-Cells via a PKA-Dependent Pathway
Islet Studies Abstract The Takeda-G-protein-receptor-5 (TGR5) mediates physiological actions of bile acids. Since it was shown that TGR5 is expressed in pancreatic tissue, a direct TGR5 activation in β-cells is currently postulated and discussed. The current study reveals that oleanolic acid (OLA) affects murine β-cell function by TGR5 activation. Both a Gαs inhibitor and an inhibitor of adenylyl cyclase (AC) prevented stimulating effects of OLA.
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