Lahari Basu, Lili Grieco-St-Pierre, Ma Enrica Angela Ching, John D H Stead, Antonio A Hanson, Jana Palaniyandi, Erin van Zyl, Myriam P Hoyeck, Kelsea S McKay, Kyle A van Allen, Hyojin Lee, Xiao-Qing Dai, Austin Bautista, Evgenia Fadzeyeva, Erin E Mulvihill, Carole L Yauk, Jan A Mennigen, Patrick E MacDonald, Jennifer E Bruin
{"title":"Cisplatin Exposure Dysregulates Insulin Secretion in Male and Female Mice.","authors":"Lahari Basu, Lili Grieco-St-Pierre, Ma Enrica Angela Ching, John D H Stead, Antonio A Hanson, Jana Palaniyandi, Erin van Zyl, Myriam P Hoyeck, Kelsea S McKay, Kyle A van Allen, Hyojin Lee, Xiao-Qing Dai, Austin Bautista, Evgenia Fadzeyeva, Erin E Mulvihill, Carole L Yauk, Jan A Mennigen, Patrick E MacDonald, Jennifer E Bruin","doi":"10.2337/db24-0419","DOIUrl":null,"url":null,"abstract":"<p><strong>Article highlights: </strong>Cancer survivors who receive cisplatin chemotherapy have an increased risk of type 2 diabetes, but the underlying mechanisms remain unclear. The aim of this study was to investigate whether cisplatin impacts β-cell health and function, thereby contributing to increased type 2 diabetes risk in cancer survivors. In vivo and in vitro cisplatin exposure dysregulated insulin secretion in male and female mice. In vitro cisplatin exposure reduced oxygen consumption, impaired β-cell exocytotic capacity, and altered expression of genes within the insulin secretion pathway in mouse islets. Understanding how chemotherapeutic drugs cause β-cell injury is critical for designing targeted interventions to reduce the risk of cancer survivors developing type 2 diabetes after treatment.</p>","PeriodicalId":93977,"journal":{"name":"Diabetes","volume":" ","pages":"528-543"},"PeriodicalIF":0.0000,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11926276/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Diabetes","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2337/db24-0419","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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Abstract
Article highlights: Cancer survivors who receive cisplatin chemotherapy have an increased risk of type 2 diabetes, but the underlying mechanisms remain unclear. The aim of this study was to investigate whether cisplatin impacts β-cell health and function, thereby contributing to increased type 2 diabetes risk in cancer survivors. In vivo and in vitro cisplatin exposure dysregulated insulin secretion in male and female mice. In vitro cisplatin exposure reduced oxygen consumption, impaired β-cell exocytotic capacity, and altered expression of genes within the insulin secretion pathway in mouse islets. Understanding how chemotherapeutic drugs cause β-cell injury is critical for designing targeted interventions to reduce the risk of cancer survivors developing type 2 diabetes after treatment.
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