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Investigating the role of mitoNEET in iron overload-induced insulin resistance

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dc.contributor.advisorSweeney, Gary
dc.contributor.authorTam, Eddie
dc.date.accessioned2023-12-08T14:28:02Z
dc.date.available2023-12-08T14:28:02Z
dc.date.issued2023-12-08
dc.date.updated2023-12-08T14:28:01Z
dc.degree.disciplineBiology
dc.degree.levelMaster's
dc.degree.nameMSc - Master of Science
dc.description.abstractExcess iron, in a process termed iron overload (IO) is closely linked to cardiovascular and metabolic diseases. Previous research has already established a causal link between IO and insulin resistance in both cardiac and skeletal muscle setting. Building upon this knowledge, the potential for mitoNEET to offer protection against IO-induced insulin resistance was investigated. The potential mechanisms underlying the protective effects of mitoNEET, which included mitochondrial dynamics, oxidative stress, and mitophagy, was also examined in H9c2 cardiac and L6 skeletal muscle cells. Using various experimental approaches including quantitative polymerase chain reaction (qPCR), western blot, fluorescent microscopy, and reporter cell lines, mitoNEET was shown to be protective against IO-induced insulin resistance. In H9c2 cells, mitoNEET provided protection by regulating mitochondrial iron and reactive oxygen species (ROS) to prevent insulin resistance. In L6 cells, mitoNEET prevented insulin resistance via regulation of mitochondrial iron, ROS, and mitochondrial fission.
dc.identifier.urihttps://hdl.handle.net/10315/41636
dc.languageen
dc.rightsAuthor owns copyright, except where explicitly noted. Please contact the author directly with licensing requests.
dc.subjectCellular biology
dc.subjectMolecular biology
dc.subjectBiochemistry
dc.subject.keywordsIron overload
dc.subject.keywordsMitochondria
dc.subject.keywordsReactive oxygen species
dc.subject.keywordsmitoNEET
dc.subject.keywordsInsulin resistance
dc.titleInvestigating the role of mitoNEET in iron overload-induced insulin resistance
dc.typeElectronic Thesis or Dissertation

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