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dc.contributor.authorStevens, Joseph Ren_US
dc.date.accessioned2016-02-20T07:00:52Z
dc.date.available2016-02-20T07:00:52Z
dc.date.issued2014-08-28en_US
dc.identifier.othervt_gsexam:3628en_US
dc.identifier.urihttp://hdl.handle.net/10919/64849
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_US
dc.format.mediumETDen_US
dc.publisherVirginia Techen_US
dc.rightsThis Item is protected by copyright and/or related rights. Some uses of this Item may be deemed fair and permitted by law even without permission from the rights holder(s), or the rights holder(s) may have licensed the work for use under certain conditions. For other uses you need to obtain permission from the rights holder(s).en_US
dc.subjectEndotoxinen_US
dc.subjectInflammationen_US
dc.subjectGlucose Metabolismen_US
dc.titleThe Effects of Low Dose Endotoxin on Glucose Homeostasisen_US
dc.typeDissertationen_US
dc.contributor.departmentHuman Nutrition, Foods, and Exerciseen_US
dc.description.degreePHDen_US
thesis.degree.namePHDen_US
thesis.degree.leveldoctoralen_US
thesis.degree.grantorVirginia Polytechnic Institute and State Universityen_US
thesis.degree.disciplineHuman Nutrition, Foods, and Exerciseen_US
dc.contributor.committeechairHulver, Matthew Wadeen_US
dc.contributor.committeememberFrisard, Madlyn Ireneen_US
dc.contributor.committeememberDavy, Kevin Pen_US
dc.contributor.committeememberGrange, Robert Wen_US
dc.contributor.committeememberLi, Liwuen_US


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