Show simple item record

dc.contributor.advisorLimesand, Sean W.en
dc.contributor.authorKelly, Amy
dc.creatorKelly, Amyen
dc.date.accessioned2017-06-30T18:07:31Z
dc.date.available2017-06-30T18:07:31Z
dc.date.issued2017
dc.identifier.urihttp://hdl.handle.net/10150/624586
dc.description.abstractWe established that acute adrenergic receptor stimulation in β-cells suppresses oxidative metabolism. This effect provides the basis for understanding how CAs reduce cell proliferation. Furthermore, the effects of acute CA on Min6 cells were distinguished from chronic CA culture using proteomics. Together, the RNAseq, qPCR and proteomic studies support a role for adrenergic receptor signaling in the regulation of proliferaton in β-cells. This work describes the genetic and proteomic profile underlying chronic adrenergic signaling and identifies CA independent suppression of β-cell growth and metabolism. Through the use of multiple models and comparative bioinformatics, we refined the list of molecular dysfunctions associated with the IUGR pathology to a set of specific and testable adrenergic targets.
dc.language.isoen_USen
dc.publisherThe University of Arizona.en
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en
dc.subjectAdrenergic Signalingen
dc.subjectDiabetesen
dc.subjectFetal Programmingen
dc.subjectIntrauterine Growth Restrictionen
dc.subjectIsleten
dc.subjectTranscriptomicsen
dc.titleAdaptations in the Pancreatic Islet Transcriptome of Intrauterine Growth Restricted Fetusesen_US
dc.typetexten
dc.typeElectronic Dissertationen
thesis.degree.grantorUniversity of Arizonaen
thesis.degree.leveldoctoralen
dc.contributor.committeememberLimesand, Sean W.en
dc.contributor.committeememberRenquist, Benjamin J.en
dc.contributor.committeememberPapas, Klearchos K.en
dc.contributor.committeememberMcCarthy, Fiona M.en
dc.contributor.committeememberBidwell, Christopher A.en
dc.description.releaseRelease after 22-May-2018en
thesis.degree.disciplineGraduate Collegeen
thesis.degree.disciplineAnimal Sciencesen
thesis.degree.namePh.D.en
refterms.dateFOA2018-05-22T00:00:00Z
html.description.abstractWe established that acute adrenergic receptor stimulation in β-cells suppresses oxidative metabolism. This effect provides the basis for understanding how CAs reduce cell proliferation. Furthermore, the effects of acute CA on Min6 cells were distinguished from chronic CA culture using proteomics. Together, the RNAseq, qPCR and proteomic studies support a role for adrenergic receptor signaling in the regulation of proliferaton in β-cells. This work describes the genetic and proteomic profile underlying chronic adrenergic signaling and identifies CA independent suppression of β-cell growth and metabolism. Through the use of multiple models and comparative bioinformatics, we refined the list of molecular dysfunctions associated with the IUGR pathology to a set of specific and testable adrenergic targets.


Files in this item

Thumbnail
Name:
azu_etd_15467_sip1_m.pdf
Size:
31.05Mb
Format:
PDF

This item appears in the following Collection(s)

Show simple item record