{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Giusti L"],"funding":["Union’s Horizon 2020 research and innovation program","Italian Ministry of University and Research","NIDDK NIH HHS","Innovative Medicines Initiative 2 Joint Undertaking","“EFPIA”, “JDRF”, and “The Leona M. and Harry B. Helmsley Charitable Trust”"],"pagination":["2465"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9368307"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(15)"],"pubmed_abstract":["Metformin, a drug widely used in type 2 diabetes (T2D), has been shown to protect human β-cells exposed to gluco- and/or lipotoxic conditions and those in islets from T2D donors. We assessed whether metformin could relieve the human β-cell stress induced by pro-inflammatory cytokines (which mediate β-cells damage in type 1 diabetes, T1D) and investigated the underlying mechanisms using shotgun proteomics. Human islets were exposed to 50 U/mL interleukin-1β plus 1000 U/mL interferon-γ for 48 h, with or without 2.4 µg/mL metformin. Glucose-stimulated insulin secretion (GSIS) and caspase 3/7 activity were studied, and a shotgun label free proteomics analysis was performed. Metformin prevented the reduction of GSIS and the activation of caspase 3/7 induced by cytokines. Proteomics analysis ide"],"journal":["Cells"],"pubmed_title":["The Protective Action of Metformin against Pro-Inflammatory Cytokine-Induced Human Islet Cell Damage and the Mechanisms Involved."],"pmcid":["PMC9368307"],"funding_grant_id":["115,797","U01 DK127786","2017KAM2R5_005","945,268"],"pubmed_authors":["Ronci M","Del Guerra S","Zuccarini M","Tesi M","Ciregia F","Lucacchini A","Cnop M","Marselli L","Giusti L","De Luca C","Marchetti P","Zallocco L","Trerotola M","Mazzoni MR","Suleiman M","Eizirik DL"],"additional_accession":[]},"is_claimable":false,"name":"The Protective Action of Metformin against Pro-Inflammatory Cytokine-Induced Human Islet Cell Damage and the Mechanisms Involved.","description":"Metformin, a drug widely used in type 2 diabetes (T2D), has been shown to protect human β-cells exposed to gluco- and/or lipotoxic conditions and those in islets from T2D donors. We assessed whether metformin could relieve the human β-cell stress induced by pro-inflammatory cytokines (which mediate β-cells damage in type 1 diabetes, T1D) and investigated the underlying mechanisms using shotgun proteomics. Human islets were exposed to 50 U/mL interleukin-1β plus 1000 U/mL interferon-γ for 48 h, with or without 2.4 µg/mL metformin. Glucose-stimulated insulin secretion (GSIS) and caspase 3/7 activity were studied, and a shotgun label free proteomics analysis was performed. Metformin prevented the reduction of GSIS and the activation of caspase 3/7 induced by cytokines. Proteomics analysis ide","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Aug","modification":"2026-05-08T03:12:57.713Z","creation":"2025-02-19T03:23:57.933Z"},"accession":"S-EPMC9368307","cross_references":{"pubmed":["35954309"],"doi":["10.3390/cells11152465"]}}