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  1. Artikel ; Online: Peeling the onion: another layer in the regulation of insulin secretion.

    Aamodt, Kristie I / Powers, Alvin C

    The Journal of clinical investigation

    2023  Band 133, Heft 8

    Abstract: Insulin secretion by pancreatic β cells is a dynamic and highly regulated process due to the central importance of insulin in enabling efficient utilization and storage of glucose. Multiple regulatory layers enable β cells to adapt to acute changes in ... ...

    Abstract Insulin secretion by pancreatic β cells is a dynamic and highly regulated process due to the central importance of insulin in enabling efficient utilization and storage of glucose. Multiple regulatory layers enable β cells to adapt to acute changes in nutrient availability as well as chronic changes in metabolic demand. While epigenetic factors have been well established as regulators of chronic β cell adaptations to insulin resistance, their role in acute adaptations in response to nutrient stimulation has been relatively unexplored. In this issue of the JCI, Wortham et al. report that short-term dynamic changes in histone modifications regulated insulin secretion and acute β cell adaptations in response to fasting and feeding cycles. These findings highlight the importance of investigating whether other epigenetic mechanisms may contribute to acute physiologic adaptations in β cells.
    Mesh-Begriff(e) Insulin Secretion ; Onions/metabolism ; Insulin/metabolism ; Glucose/metabolism ; Insulin Resistance/physiology ; Insulin-Secreting Cells/metabolism
    Chemische Substanzen Insulin ; Glucose (IY9XDZ35W2)
    Sprache Englisch
    Erscheinungsdatum 2023-04-17
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI169718
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Peeling the onion

    Kristie I. Aamodt / Alvin C. Powers

    The Journal of Clinical Investigation, Vol 133, Iss

    another layer in the regulation of insulin secretion

    2023  Band 8

    Abstract: Insulin secretion by pancreatic β cells is a dynamic and highly regulated process due to the central importance of insulin in enabling efficient utilization and storage of glucose. Multiple regulatory layers enable β cells to adapt to acute changes in ... ...

    Abstract Insulin secretion by pancreatic β cells is a dynamic and highly regulated process due to the central importance of insulin in enabling efficient utilization and storage of glucose. Multiple regulatory layers enable β cells to adapt to acute changes in nutrient availability as well as chronic changes in metabolic demand. While epigenetic factors have been well established as regulators of chronic β cell adaptations to insulin resistance, their role in acute adaptations in response to nutrient stimulation has been relatively unexplored. In this issue of the JCI, Wortham et al. report that short-term dynamic changes in histone modifications regulated insulin secretion and acute β cell adaptations in response to fasting and feeding cycles. These findings highlight the importance of investigating whether other epigenetic mechanisms may contribute to acute physiologic adaptations in β cells.
    Schlagwörter Medicine ; R
    Sprache Englisch
    Erscheinungsdatum 2023-04-01T00:00:00Z
    Verlag American Society for Clinical Investigation
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: Signals in the pancreatic islet microenvironment influence β-cell proliferation.

    Aamodt, Kristie I / Powers, Alvin C

    Diabetes, obesity & metabolism

    2017  Band 19 Suppl 1, Seite(n) 124–136

    Abstract: The progressive loss of pancreatic β-cell mass that occurs in both type 1 and type 2 diabetes is a primary factor driving efforts to identify strategies for effectively increasing, enhancing or restoring β-cell mass. While factors that seem to influence ... ...

    Abstract The progressive loss of pancreatic β-cell mass that occurs in both type 1 and type 2 diabetes is a primary factor driving efforts to identify strategies for effectively increasing, enhancing or restoring β-cell mass. While factors that seem to influence β-cell proliferation in specific contexts have been described, reliable stimulation of human β-cell proliferation has remained a challenge. Importantly, β-cells exist in the context of a complex, integrated pancreatic islet microenvironment where they interact with other endocrine cells, vascular endothelial cells, extracellular matrix, neuronal projections and islet macrophages. This review highlights different components of the pancreatic microenvironment, and reviews what is known about how signaling that occurs between β-cells and these other components influences β-cell proliferation. Future efforts to further define the role of the pancreatic islet microenvironment on β-cell proliferation may lead to the development of successful approaches to increase or restore β-cell mass in diabetes.
    Mesh-Begriff(e) Animals ; Apoptosis ; Cell Communication ; Cell Proliferation ; Cellular Microenvironment ; Diabetes Mellitus, Type 1/metabolism ; Diabetes Mellitus, Type 1/pathology ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/pathology ; Extracellular Matrix/immunology ; Extracellular Matrix/metabolism ; Extracellular Matrix/pathology ; Glucagon-Secreting Cells/cytology ; Glucagon-Secreting Cells/immunology ; Glucagon-Secreting Cells/metabolism ; Glucagon-Secreting Cells/pathology ; Humans ; Insulin-Secreting Cells/cytology ; Insulin-Secreting Cells/immunology ; Insulin-Secreting Cells/metabolism ; Insulin-Secreting Cells/pathology ; Islets of Langerhans/blood supply ; Islets of Langerhans/cytology ; Islets of Langerhans/innervation ; Islets of Langerhans/pathology ; Macrophages/cytology ; Macrophages/immunology ; Macrophages/metabolism ; Macrophages/pathology ; Models, Biological ; Pancreatic Polypeptide-Secreting Cells/cytology ; Pancreatic Polypeptide-Secreting Cells/immunology ; Pancreatic Polypeptide-Secreting Cells/metabolism ; Pancreatic Polypeptide-Secreting Cells/pathology ; Somatostatin-Secreting Cells/cytology ; Somatostatin-Secreting Cells/immunology ; Somatostatin-Secreting Cells/metabolism ; Somatostatin-Secreting Cells/pathology ; Species Specificity
    Sprache Englisch
    Erscheinungsdatum 2017-09-06
    Erscheinungsland England
    Dokumenttyp Journal Article ; Review ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
    ZDB-ID 1454944-x
    ISSN 1463-1326 ; 1462-8902
    ISSN (online) 1463-1326
    ISSN 1462-8902
    DOI 10.1111/dom.13031
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Coordinated interactions between endothelial cells and macrophages in the islet microenvironment promote β cell regeneration.

    Saunders, Diane C / Aamodt, Kristie I / Richardson, Tiffany M / Hopkirk, Alexander J / Aramandla, Radhika / Poffenberger, Greg / Jenkins, Regina / Flaherty, David K / Prasad, Nripesh / Levy, Shawn E / Powers, Alvin C / Brissova, Marcela

    NPJ Regenerative medicine

    2021  Band 6, Heft 1, Seite(n) 22

    Abstract: Endogenous β cell regeneration could alleviate diabetes, but proliferative stimuli within the islet microenvironment are incompletely understood. We previously found that β cell recovery following hypervascularization-induced β cell loss involves ... ...

    Abstract Endogenous β cell regeneration could alleviate diabetes, but proliferative stimuli within the islet microenvironment are incompletely understood. We previously found that β cell recovery following hypervascularization-induced β cell loss involves interactions with endothelial cells (ECs) and macrophages (MΦs). Here we show that proliferative ECs modulate MΦ infiltration and phenotype during β cell loss, and recruited MΦs are essential for β cell recovery. Furthermore, VEGFR2 inactivation in quiescent ECs accelerates islet vascular regression during β cell recovery and leads to increased β cell proliferation without changes in MΦ phenotype or number. Transcriptome analysis of β cells, ECs, and MΦs reveals that β cell proliferation coincides with elevated expression of extracellular matrix remodeling molecules and growth factors likely driving activation of proliferative signaling pathways in β cells. Collectively, these findings suggest a new β cell regeneration paradigm whereby coordinated interactions between intra-islet MΦs, ECs, and extracellular matrix mediate β cell self-renewal.
    Sprache Englisch
    Erscheinungsdatum 2021-04-06
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ISSN 2057-3995
    ISSN (online) 2057-3995
    DOI 10.1038/s41536-021-00129-z
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Coordinated interactions between endothelial cells and macrophages in the islet microenvironment promote β cell regeneration

    Diane C. Saunders / Kristie I. Aamodt / Tiffany M. Richardson / Alexander J. Hopkirk / Radhika Aramandla / Greg Poffenberger / Regina Jenkins / David K. Flaherty / Nripesh Prasad / Shawn E. Levy / Alvin C. Powers / Marcela Brissova

    npj Regenerative Medicine, Vol 6, Iss 1, Pp 1-

    2021  Band 13

    Abstract: Abstract Endogenous β cell regeneration could alleviate diabetes, but proliferative stimuli within the islet microenvironment are incompletely understood. We previously found that β cell recovery following hypervascularization-induced β cell loss ... ...

    Abstract Abstract Endogenous β cell regeneration could alleviate diabetes, but proliferative stimuli within the islet microenvironment are incompletely understood. We previously found that β cell recovery following hypervascularization-induced β cell loss involves interactions with endothelial cells (ECs) and macrophages (MΦs). Here we show that proliferative ECs modulate MΦ infiltration and phenotype during β cell loss, and recruited MΦs are essential for β cell recovery. Furthermore, VEGFR2 inactivation in quiescent ECs accelerates islet vascular regression during β cell recovery and leads to increased β cell proliferation without changes in MΦ phenotype or number. Transcriptome analysis of β cells, ECs, and MΦs reveals that β cell proliferation coincides with elevated expression of extracellular matrix remodeling molecules and growth factors likely driving activation of proliferative signaling pathways in β cells. Collectively, these findings suggest a new β cell regeneration paradigm whereby coordinated interactions between intra-islet MΦs, ECs, and extracellular matrix mediate β cell self-renewal.
    Schlagwörter Medicine ; R
    Sprache Englisch
    Erscheinungsdatum 2021-04-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  6. Artikel ; Online: Development of a reliable automated screening system to identify small molecules and biologics that promote human β-cell regeneration.

    Aamodt, Kristie I / Aramandla, Radhika / Brown, Judy J / Fiaschi-Taesch, Nathalie / Wang, Peng / Stewart, Andrew F / Brissova, Marcela / Powers, Alvin C

    American journal of physiology. Endocrinology and metabolism

    2016  Band 311, Heft 5, Seite(n) E859–E868

    Abstract: Numerous compounds stimulate rodent β-cell proliferation; however, translating these findings to human β-cells remains a challenge. To examine human β-cell proliferation in response to such compounds, we developed a medium-throughput in vitro method of ... ...

    Abstract Numerous compounds stimulate rodent β-cell proliferation; however, translating these findings to human β-cells remains a challenge. To examine human β-cell proliferation in response to such compounds, we developed a medium-throughput in vitro method of quantifying adult human β-cell proliferation markers. This method is based on high-content imaging of dispersed islet cells seeded in 384-well plates and automated cell counting that identifies fluorescently labeled β-cells with high specificity using both nuclear and cytoplasmic markers. β-Cells from each donor were assessed for their function and ability to enter the cell cycle by cotransduction with adenoviruses encoding cell cycle regulators cdk6 and cyclin D3. Using this approach, we tested 12 previously identified mitogens, including neurotransmitters, hormones, growth factors, and molecules, involved in adenosine and Tgf-1β signaling. Each compound was tested in a wide concentration range either in the presence of basal (5 mM) or high (11 mM) glucose. Treatment with the control compound harmine, a Dyrk1a inhibitor, led to a significant increase in Ki-67
    Mesh-Begriff(e) Activins/pharmacology ; Adenosine/analogs & derivatives ; Adenosine/pharmacology ; Adenosine A2 Receptor Agonists/pharmacology ; Adenosine-5'-(N-ethylcarboxamide)/pharmacology ; Adult ; Automation ; Cell Culture Techniques ; Cell Proliferation/drug effects ; Drug Evaluation, Preclinical ; Erythropoietin/pharmacology ; Exenatide ; Female ; GABA Agents/pharmacology ; Harmine/pharmacology ; Humans ; Incretins/pharmacology ; Insulin-Secreting Cells/drug effects ; Male ; Middle Aged ; Monoamine Oxidase Inhibitors/pharmacology ; Myostatin/pharmacology ; Nucleosides/pharmacology ; Peptides/pharmacology ; Platelet-Derived Growth Factor/pharmacology ; Prolactin/pharmacology ; Regeneration/drug effects ; Serotonin/pharmacology ; Serotonin Receptor Agonists/pharmacology ; Vasodilator Agents/pharmacology ; Venoms/pharmacology ; Young Adult ; gamma-Aminobutyric Acid/pharmacology
    Chemische Substanzen A 134974 ; Adenosine A2 Receptor Agonists ; GABA Agents ; Incretins ; Monoamine Oxidase Inhibitors ; Myostatin ; Nucleosides ; Peptides ; Platelet-Derived Growth Factor ; Serotonin Receptor Agonists ; UK-432097 ; Vasodilator Agents ; Venoms ; activin A ; Activins (104625-48-1) ; Erythropoietin (11096-26-7) ; Serotonin (333DO1RDJY) ; Adenosine-5'-(N-ethylcarboxamide) (35920-39-9) ; Harmine (4FHH5G48T7) ; gamma-Aminobutyric Acid (56-12-2) ; Prolactin (9002-62-4) ; Exenatide (9P1872D4OL) ; Adenosine (K72T3FS567)
    Sprache Englisch
    Erscheinungsdatum 2016-09-13
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 603841-4
    ISSN 1522-1555 ; 0193-1849
    ISSN (online) 1522-1555
    ISSN 0193-1849
    DOI 10.1152/ajpendo.00515.2015
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Uc I Zs.89: Hefte anzeigen Standort:
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  7. Artikel ; Online: Interrupted Glucagon Signaling Reveals Hepatic α Cell Axis and Role for L-Glutamine in α Cell Proliferation.

    Dean, E Danielle / Li, Mingyu / Prasad, Nripesh / Wisniewski, Scott N / Von Deylen, Alison / Spaeth, Jason / Maddison, Lisette / Botros, Anthony / Sedgeman, Leslie R / Bozadjieva, Nadejda / Ilkayeva, Olga / Coldren, Anastasia / Poffenberger, Greg / Shostak, Alena / Semich, Michael C / Aamodt, Kristie I / Phillips, Neil / Yan, Hai / Bernal-Mizrachi, Ernesto /
    Corbin, Jackie D / Vickers, Kasey C / Levy, Shawn E / Dai, Chunhua / Newgard, Christopher / Gu, Wei / Stein, Roland / Chen, Wenbiao / Powers, Alvin C

    Cell metabolism

    2017  Band 25, Heft 6, Seite(n) 1362–1373.e5

    Abstract: Decreasing glucagon action lowers the blood glucose and may be useful therapeutically for diabetes. However, interrupted glucagon signaling leads to α cell proliferation. To identify postulated hepatic-derived circulating factor(s) responsible for α cell ...

    Abstract Decreasing glucagon action lowers the blood glucose and may be useful therapeutically for diabetes. However, interrupted glucagon signaling leads to α cell proliferation. To identify postulated hepatic-derived circulating factor(s) responsible for α cell proliferation, we used transcriptomics/proteomics/metabolomics in three models of interrupted glucagon signaling and found that proliferation of mouse, zebrafish, and human α cells was mTOR and FoxP transcription factor dependent. Changes in hepatic amino acid (AA) catabolism gene expression predicted the observed increase in circulating AAs. Mimicking these AA levels stimulated α cell proliferation in a newly developed in vitro assay with L-glutamine being a critical AA. α cell expression of the AA transporter Slc38a5 was markedly increased in mice with interrupted glucagon signaling and played a role in α cell proliferation. These results indicate a hepatic α islet cell axis where glucagon regulates serum AA availability and AAs, especially L-glutamine, regulate α cell proliferation and mass via mTOR-dependent nutrient sensing.
    Mesh-Begriff(e) Amino Acid Transport Systems, Neutral/genetics ; Amino Acid Transport Systems, Neutral/metabolism ; Animals ; Cell Proliferation ; Glucagon/genetics ; Glucagon/metabolism ; Glutamine/genetics ; Glutamine/metabolism ; Liver/metabolism ; Mice ; Mice, Knockout ; Signal Transduction ; Zebrafish ; Zebrafish Proteins/genetics ; Zebrafish Proteins/metabolism
    Chemische Substanzen Amino Acid Transport Systems, Neutral ; SNAT5 protein, mouse ; Zebrafish Proteins ; Glutamine (0RH81L854J) ; Glucagon (9007-92-5)
    Sprache Englisch
    Erscheinungsdatum 2017-06-07
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2176834-1
    ISSN 1932-7420 ; 1550-4131
    ISSN (online) 1932-7420
    ISSN 1550-4131
    DOI 10.1016/j.cmet.2017.05.011
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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