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dc.contributor.authorAli, Mohammed Irfan
dc.date.accessioned2014-05-07T19:22:55Z
dc.date.available2014-05-07T19:22:55Z
dc.date.issued2010-07en
dc.identifier.urihttp://hdl.handle.net/10675.2/316604
dc.description.abstractThe overall goal of the current study was to determine if improving the net glycemic load and lipid derangements associated with IR in obesity by genetically deleting PTP1B in a mouse model of obesity would improve microvascular function.
dc.relation.urlhttp://ezproxy.augusta.edu/login?url=https://search.proquest.com/docview/750079326?accountid=12365en
dc.rightsAccess restricted to authorized Georgia Regents University users only.en
dc.subjectCardiovascular Dysfunctionen
dc.subjectObesityen
dc.subjectInsulinen
dc.subjectProtein Tyrosine Phosphatase 1Ben
dc.subjectGlycerinen
dc.subjectMicrovascularen
dc.titlePeripheral Insulin Resistance Mediates Microvascular Dysfunction in Obese Mice via Increase NAD(P)H Oxidase Isoform one Mediated Superoxide Productionen
dc.typeDissertationen
dc.contributor.departmentDepartment of Physiologyen
dc.contributor.corporatenameGeorgia Regents Universityen
dc.description.advisorNot Listeden
dc.description.degreeDoctor of Philosophy (Ph.D.)en
dc.description.committeeNot Listeden
html.description.abstractThe overall goal of the current study was to determine if improving the net glycemic load and lipid derangements associated with IR in obesity by genetically deleting PTP1B in a mouse model of obesity would improve microvascular function.


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