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dc.contributor.advisorLacombe, Veronique
dc.contributor.advisorLyvers-Peffer, Pasha
dc.creatorKohler, Kaleb
dc.date.accessioned2011-05-25T16:55:33Z
dc.date.available2011-05-25T16:55:33Z
dc.date.issued2011-06
dc.identifier.urihttp://hdl.handle.net/1811/48846
dc.description.abstractAlthough the importance of adipose tissue (AT) glucose transport in regulating systemic insulin sensitivity is becoming increasingly evident and insulin resistance (IR) has been widely recognized, the underlying alterations in glucose transport and its contributions to IR are still not well understood. The purpose of the present study was to determine the early pathological changes in glucose transport by characterizing alterations in glucose transporters (GLUTs) in visceral and subcutaneous adipose depots in a novel equine model of naturally occurring compensated IR. AT biopsies were collected from horses, which were classified as insulin-sensitive (IS) or compensated IR based on the results of an insulin-modified frequently sampled intravenous glucose tolerance test. Protein expression of GLUT-4 (major isoform) and GLUT-12 (a newly discovered isoform) were measured by Western blotting in visceral and subcutaneous adipose depots, along with AS160 (a potential key protein in GLUT cell-surface trafficking). Using a biotinylated bis-mannose photolabel technique, active cell surface GLUT-4 and-12 content was also quantified to estimate GLUT trafficking. Omental AT had the highest total GLUT-4 and GLUT-12 content compared to other sites during the IS state. IR was associated with a significantly reduced total GLUT-4, but not GLUT-12, content in omental AT, without a change in content in the other adipose sites. In addition, active cell surface GLUT-4, but not -12, was lower in subcutaneous and visceral AT of IR compared to IS horses. Impairment in GLUT-4 trafficking occurred independently of any changes in AS160 phosphorlyation between groups. The data suggests that GLUT-4, but not -12, is a pathogenic factor in AT during naturally occurring compensated IR, despite normal AS160 activation.en_US
dc.description.sponsorshipCollege of Food, Agriculture, and Environmental Sciences Undergraduate Research Granten_US
dc.language.isoen_USen_US
dc.publisherThe Ohio State Universityen_US
dc.relation.ispartofseriesThe Ohio State University. Department of Animal Sciences Honors Theses; 2011en_US
dc.subjectAS160en_US
dc.subjectInsulin Resistanceen_US
dc.subjectAdipose Tissueen_US
dc.subjectGLUT-4en_US
dc.subjectGLUT-12en_US
dc.titleRegulation of the Glucose Transport Pathway in Adipose Tissue of Horses with Insulin Resistanceen_US
dc.typeThesisen_US
dc.description.embargoNo embargoen_US


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