{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kabra UD"],"funding":["Novo Nordisk Foundation"],"pagination":["12338"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9604375"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["23(20)"],"pubmed_abstract":["Mitochondrial dynamics and bioenergetics are central to glucose-stimulated insulin secretion by pancreatic beta cells. Previously, we demonstrated that a disturbance in glucose-invoked fission impairs insulin secretion by compromising glucose catabolism. Here, we investigated whether the overexpression of mitochondrial fission regulator <i>Drp1</i> in MIN6 cells can improve or rescue insulin secretion. Although <i>Drp1</i> overexpression slightly improves the triggering mechanism of insulin secretion of the <i>Drp1</i>-knockdown cells and has no adverse effects on mitochondrial metabolism in wildtype MIN6 cells, the constitutive presence of <i>Drp1</i> unexpectedly impairs insulin content, which leads to a reduction in the absolute values of secreted insulin. Coherent with previous studies in <i>Drp1</i>-overexpressing muscle cells, we found that the upregulation of ER stress-related genes (<i>BiP</i>, <i>Chop</i>, and <i>Hsp60</i>) possibly impacts insulin production in MIN6 cells. Collectively, we confirm the important role of <i>Drp1</i> for the energy-coupling of insulin secretion but unravel off-targets effects by <i>Drp1</i> overexpression on insulin content that warrant caution when manipulating <i>Drp1</i> in disease therapy."],"journal":["International journal of molecular sciences"],"pubmed_title":["Drp1 Overexpression Decreases Insulin Content in Pancreatic MIN6 Cells."],"pmcid":["PMC9604375"],"funding_grant_id":["0059646"],"pubmed_authors":["Jastroch M","Kabra UD","Moruzzi N","Berggren PO"],"additional_accession":[]},"is_claimable":false,"name":"Drp1 Overexpression Decreases Insulin Content in Pancreatic MIN6 Cells.","description":"Mitochondrial dynamics and bioenergetics are central to glucose-stimulated insulin secretion by pancreatic beta cells. Previously, we demonstrated that a disturbance in glucose-invoked fission impairs insulin secretion by compromising glucose catabolism. Here, we investigated whether the overexpression of mitochondrial fission regulator <i>Drp1</i> in MIN6 cells can improve or rescue insulin secretion. Although <i>Drp1</i> overexpression slightly improves the triggering mechanism of insulin secretion of the <i>Drp1</i>-knockdown cells and has no adverse effects on mitochondrial metabolism in wildtype MIN6 cells, the constitutive presence of <i>Drp1</i> unexpectedly impairs insulin content, which leads to a reduction in the absolute values of secreted insulin. Coherent with previous studies in <i>Drp1</i>-overexpressing muscle cells, we found that the upregulation of ER stress-related genes (<i>BiP</i>, <i>Chop</i>, and <i>Hsp60</i>) possibly impacts insulin production in MIN6 cells. Collectively, we confirm the important role of <i>Drp1</i> for the energy-coupling of insulin secretion but unravel off-targets effects by <i>Drp1</i> overexpression on insulin content that warrant caution when manipulating <i>Drp1</i> in disease therapy.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Oct","modification":"2025-04-04T11:29:28.576Z","creation":"2025-04-04T11:29:28.576Z"},"accession":"S-EPMC9604375","cross_references":{"pubmed":["36293194"],"doi":["10.3390/ijms232012338"]}}