{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T15:50:30Z","timestamp":1791561030653,"version":"4.3.4"},"reference-count":49,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T00:00:00Z","timestamp":1791504000000},"content-version":"vor","delay-in-days":8,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T00:00:00Z","timestamp":1790812800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Archiv der Pharmazie"],"published-print":{"date-parts":[[2026,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Metabolic stress increases the whole\u2010cell current through K\n                    <jats:sub>Ca<\/jats:sub>\n                    3.1 channels in mouse pancreatic islet cells. The study aimed to analyze the network between ion channels mediating Ca\n                    <jats:sup>2+<\/jats:sup>\n                    influx for K\n                    <jats:sub>Ca<\/jats:sub>\n                    3.1 channel activation and stress\u2010related changes. The physiologically important K\n                    <jats:sub>slow<\/jats:sub>\n                    current of beta cells was not altered in total but the contribution of K\n                    <jats:sub>Ca<\/jats:sub>\n                    3.1 current was reduced after culture in the presence of high glucose and palmitate concentrations. Electrical activity was increased by blocking K\n                    <jats:sub>Ca<\/jats:sub>\n                    3.1 channels with senicapoc in islets cultured under standard conditions but not after metabolic stress. Of note, the functional coupling of K\n                    <jats:sub>Ca<\/jats:sub>\n                    3.1 to\n                    <jats:sc>l<\/jats:sc>\n                    \u2010type Ca\n                    <jats:sup>2+<\/jats:sup>\n                    channels was severely reduced by metabolic stress, whereas the coupling to Ca\n                    <jats:sup>2+<\/jats:sup>\n                    \u2010influx via NMDA receptors increased. Mitochondrial membrane potential of beta cells was not affected by senicapoc but by a mitochondria\u2010targeted derivative. Inhibition of K\n                    <jats:sub>Ca<\/jats:sub>\n                    3.1 channels by senicapoc or maurotoxin partly protected from apoptosis. In conclusion, the data indicate a shift in the interplay of Ca\n                    <jats:sup>2+<\/jats:sup>\n                    \u2010conducting ion channels and the plasma membrane\u2010localized K\n                    <jats:sub>Ca<\/jats:sub>\n                    3.1 channel. K\n                    <jats:sub>Ca<\/jats:sub>\n                    3.1 channels changed from an important regulator of membrane potential oscillations to a dysfunctional and proapoptotic factor. This switch might be involved in the decline of islet cell mass and function during progression of type 2 diabetes mellitus.\n                  <\/jats:p>","DOI":"10.1002\/ardp.70344","type":"journal-article","created":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T15:08:14Z","timestamp":1791558494000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Metabolic Stress Shifts the Function of K\n                    <sub>Ca<\/sub>\n                    3.1 Channels in Pancreatic Beta Cells From a Regulator of Membrane Potential to a Proapoptotic Factor"],"prefix":"10.1002","volume":"359","author":[{"given":"Jurek","family":"Hense","sequence":"first","affiliation":[{"name":"Institute of Pharmaceutical and Medicinal Chemistry, Department of Pharmacology University of M\u00fcnster M\u00fcnster 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