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  • American Physiological Society  (3)
  • 1
    Online Resource
    Online Resource
    On-line analysis of gap junctions reveals more efficient electrical than dye coupling between islet cells
    American Physiological Society ; 2003
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 284, No. 5 ( 2003-05-01), p. E980-E987
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 284, No. 5 ( 2003-05-01), p. E980-E987
    Abstract: Pancreatic β-cells constitute a well-communicating multicellular network that permits a coordinated and synchronized signal transmission within the islet of Langerhans that is necessary for proper insulin release. Gap junctions are the molecular keys that mediate functional cellular connections, which are responsible for electrical and metabolic coupling in the majority of cell types. Although the role of gap junctions in β-cell electrical coupling is well documented, metabolic communication is still a matter of discussion. Here, we have addressed this issue by use of a fluorescence recovery after photobleaching (FRAP) approach. This technique has been validated as a reliable and noninvasive approach to monitor functional gap junctions in real time. We show that control pancreatic islet cells did not exchange a gap junction-permeant molecule in either clustered cells or intact islets of Langerhans under conditions that allowed cell-to-cell exchange of current-carrying ions. Conversely, we have detected that the same probe was extensively transferred between islet cells of transgenic mice expressing connexin 32 (Cx32) that have enhanced junctional coupling properties. The results indicate that the electrical coupling of native islet cells is more extensive than dye communication. Dye-coupling domains in islet cells appear more restricted than previously inferred with other methods.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.00473.2002
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2003
    detail.hit.zdb_id: 1477331-4
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  • 2
    Online Resource
    Online Resource
    Endocrine disruptors in plastics alter β-cell physiology and increase the risk of diabetes mellitus
    American Physiological Society ; 2023
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 324, No. 6 ( 2023-06-01), p. E488-E505
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 324, No. 6 ( 2023-06-01), p. E488-E505
    Abstract: Plastic pollution breaks a planetary boundary threatening wildlife and humans through its physical and chemical effects. Of the latter, the release of endocrine disrupting chemicals (EDCs) has consequences on the prevalence of human diseases related to the endocrine system. Bisphenols (BPs) and phthalates are two groups of EDCs commonly found in plastics that migrate into the environment and make low-dose human exposure ubiquitous. Here we review epidemiological, animal, and cellular studies linking exposure to BPs and phthalates to altered glucose regulation, with emphasis on the role of pancreatic β-cells. Epidemiological studies indicate that exposure to BPs and phthalates is associated with diabetes mellitus. Studies in animal models indicate that treatment with doses within the range of human exposure decreases insulin sensitivity and glucose tolerance, induces dyslipidemia, and modifies functional β-cell mass and serum levels of insulin, leptin, and adiponectin. These studies reveal that disruption of β-cell physiology by EDCs plays a key role in impairing glucose homeostasis by altering the mechanisms used by β-cells to adapt to metabolic stress such as chronic nutrient excess. Studies at the cellular level demonstrate that BPs and phthalates modify the same biochemical pathways involved in adaptation to chronic excess fuel. These include changes in insulin biosynthesis and secretion, electrical activity, expression of key genes, and mitochondrial function. The data summarized here indicate that BPs and phthalates are important risk factors for diabetes mellitus and support a global effort to decrease plastic pollution and human exposure to EDCs.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.00068.2023
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2023
    detail.hit.zdb_id: 1477331-4
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Inhibition of Ca 2+ signaling and glucagon secretion in mouse pancreatic α-cells by extracellular ATP and purinergic receptors
    American Physiological Society ; 2008
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 294, No. 5 ( 2008-05), p. E952-E960
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 294, No. 5 ( 2008-05), p. E952-E960
    Abstract: Glucagon secreted from pancreatic α-cells plays a critical role in glycemia, mainly by hepatic glucose mobilization. In diabetic patients, an impaired control of glucagon release can worsen glucose homeostasis. Despite its importance, the mechanisms that regulate its secretion are still poorly understood. Since α-cells are particularly sensitive to neural and paracrine factors, in this report we studied the role of purinergic receptors and extracellular ATP, which can be released from nerve terminals and β-cell secretory granules. Using immunocytochemistry, we identified in α-cells the P2 receptor subtype P2Y 1 , as well as the P1 receptors A 1 and A 2A . In contrast, only P2Y 1 and A 1 receptors were localized in β-cells. To analyze the role of purinergic receptors in α-cell function, we studied their participation in Ca 2+ signaling. At low glucose concentrations, mouse α-cells exhibited the characteristic oscillatory Ca 2+ signals that lead to secretion. Application of ATP (1–10 μM) abolished these oscillations or reduced their frequency in α-cells within intact islets and isolated in culture. ATPγS, a nonhydrolyzable ATP derivative, indicated that the ATP effect was mainly direct rather than through ATP-hydrolytic products. Additionally, adenosine (1–10 μM) was also found to reduce Ca 2+ signals. ATP-mediated inhibition of Ca 2+ signaling was accompanied by a decrease in glucagon release from intact islets in contrast to the adenosine effect. Using pharmacological agonists, we found that only P2Y 1 and A 2A were likely involved in the inhibitory effect on Ca 2+ signaling. All these findings indicate that extracellular ATP and purinergic stimulation are effective regulators of the α-cell function.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.00641.2007
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2008
    detail.hit.zdb_id: 1477331-4
    SSG: 12
    Location Call Number Limitation Availability
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    Online Resource
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