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dc.contributor.authorStevens, Joseph R.en
dc.date.accessioned2016-02-20T07:00:52Zen
dc.date.available2016-02-20T07:00:52Zen
dc.date.issued2014-08-28en
dc.identifier.othervt_gsexam:3628en
dc.identifier.urihttp://hdl.handle.net/10919/64849en
dc.description.abstractObese individuals present with an increased inflammatory tone as compared to healthy, normal-weight individuals, which is associated with insulin resistance. One factor hypothesized to contribute to increased inflammation in obese and diabetic states is elevated blood endotoxin levels, also known as metabolic endotoxemia. In healthy rodents (non-obese and insulin sensitive), there is evidence that blood endotoxin levels fluctuate over the course of the day with elevations in the post-prandial state that return to baseline levels in the post-absorptive state. High-fat feeding in these animals altered these fluctuations causing endotoxin levels to remain high throughout the day. The effects of alterations in endotoxin levels on glucose metabolism are not understood. The goal of this study was to determine the effects of short-term and long-term increases in endotoxin of a low magnitude on insulin signaling in a human primary cell line as well as the effects of short-term endotoxin treatments on glucose homeostasis in a C57/Bl6 mouse model. First, we tested the hypothesis in cell culture that short-term low-dose endotoxin treatments would enhance insulin-signaling and glycogen synthesis while long-term treatments would have inhibitory effects. Under our second hypothesis, we examined whether short-term low-dose treatments of endotoxin would contribute to improvements in glucose tolerance in a mouse model. In contrast to our first hypothesis, short-term endotoxin treatments did not improve insulin signaling or glycogen synthesis although long-term treatments did contribute to decreases in glycogen synthesis. Interestingly, short-term endotoxin treatments resulted in significant improvements in glucose clearance in the mouse model; this is believed to be partly attributed to LPS inhibiting gluconeogenesis. Future studies are necessary to understand the mechanisms responsible for altered glucose metabolism in response to low magnitude changes in LPS levels.en
dc.format.mediumETDen
dc.publisherVirginia Techen
dc.rightsIn Copyrighten
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/en
dc.subjectEndotoxinen
dc.subjectInflammationen
dc.subjectGlucose Metabolismen
dc.titleThe Effects of Low Dose Endotoxin on Glucose Homeostasisen
dc.typeDissertationen
dc.contributor.departmentHuman Nutrition, Foods, and Exerciseen
dc.description.degreePh. D.en
thesis.degree.namePh. D.en
thesis.degree.leveldoctoralen
thesis.degree.grantorVirginia Polytechnic Institute and State Universityen
thesis.degree.disciplineHuman Nutrition, Foods, and Exerciseen
dc.contributor.committeechairHulver, Matthew W.en
dc.contributor.committeememberFrisard, Madlyn I.en
dc.contributor.committeememberDavy, Kevin P.en
dc.contributor.committeememberGrange, Robert W.en
dc.contributor.committeememberLi, Liwuen


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