Thesis (Ph.D.)--University of Western Australia, 2006.

Thesis (M. S. in Molecular Physiology and Biophysics)--Vanderbilt University, Aug. 2008. / Title from title screen. Includes bibliographical references.

Thesis (M.Sc.)--York University, 2008. Graduate Programme in Kinesiology and Health Science. / Typescript. Includes bibliographical references (leaves 49-64). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:MR51527

Thesis (Ph. D.)--University of Wisconsin--Madison, 1965. / Typescript. Vita. Description based on print version record. Includes bibliographical references.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1969. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliography.

No description available.

BACKGROUND: Post-bariatric hypoglycemia (PBH), a complication of gastric bypass surgery, is characterized by postprandial hyperinsulinemic hypoglycemia. To date, the etiology of PBH has not been fully elucidated. OBJECTIVE: To develop a murine model of PBH by experimentally modifying candidate molecules identified in humans with PBH. METHODS: Gastric bypass patients were assigned to groups based on whether or not they suffered from hypoglycemia (PBH, n = 11; asymptomatic, n = 7). Patients underwent a mixed meal tolerance test with blood draws at baseline, 30 minutes, and 120 minutes postprandially. SOMAscan (Somalogic) was used to evaluate serum for protein levels. In parallel, mass spectrometry (Metabolon) was used to examine metabolite levels. Mice were treated with the Farnesoid X Receptor (FXR) agonist, fexaramine (Fex), or vehicle for 5 days before undergoing a glucose tolerance test (GTT). Mice were sacrificed with tissues collected immediately thereafter. PCR was performed to quantify expression of FXR target genes. A separate cohort of mice was treated with adenine or vehicle for 2 days before undergoing a GTT or an insulin tolerance test. RESULTS: FGF19 was the most significantly upregulated protein in the PBH group at all time points. At 120 minutes postprandially, FGF19 was 2.1-fold higher in the PBH group (p < 1x10-5). Adenine was >2-fold higher at all time points (p < 1x10-8). Treatment with Fex did not result in significant differences during GTT or in expression of FXR target genes. Treatment with adenine did not significantly impact glucose tolerance or insulin sensitivity between groups. CONCLUSIONS: The results of the human serum analyses established a strong foundation on which to develop a murine model of PBH. Though the mouse experiments failed to induce postprandial hypoglycemia, they have directed future experiments toward developing a murine model of PBH. / 2018-07-11T00:00:00Z

Thesis (Ph. D.)--University of Washington, 2001. / Vita. Includes bibliographical references (leaves 152-175).

Severe hypoglycemia poses the greatest challenge to glycemic control in diabetic patients, especially children with type 1 diabetes mellitus. Although in vivo animal models exist for investigating the effects of hypoglycemia, few studies examine repeated hypoglycemia and none investigate within the context of a juvenile animal model. The main objective of this thesis was to examine electroencephalographic (EEG) and behavioral abnormalities manifesting as a result of repeated hypoglycemia in juvenile diabetic and non-diabetic mouse models. Using a novel implantation technique, the hippocampal and cortical EEG were recorded during repeated insulin-induced hypoglycemia. It was discovered that repeated hypoglycemia exacerbated behavioral convulsion severity and promoted epileptiform EEG activity within the hippocampus and cortex of both diabetic and non-diabetic animals. Furthermore, sustained hypoglycemia caused a significant decrease in hippocampal EEG activity in diabetic animals compared with non-diabetics. These results suggest recurrent hypoglycemia may promote and worsen seizures associated with hypoglycemia in diabetic children.

Severe hypoglycemia poses the greatest challenge to glycemic control in diabetic patients, especially children with type 1 diabetes mellitus. Although in vivo animal models exist for investigating the effects of hypoglycemia, few studies examine repeated hypoglycemia and none investigate within the context of a juvenile animal model. The main objective of this thesis was to examine electroencephalographic (EEG) and behavioral abnormalities manifesting as a result of repeated hypoglycemia in juvenile diabetic and non-diabetic mouse models. Using a novel implantation technique, the hippocampal and cortical EEG were recorded during repeated insulin-induced hypoglycemia. It was discovered that repeated hypoglycemia exacerbated behavioral convulsion severity and promoted epileptiform EEG activity within the hippocampus and cortex of both diabetic and non-diabetic animals. Furthermore, sustained hypoglycemia caused a significant decrease in hippocampal EEG activity in diabetic animals compared with non-diabetics. These results suggest recurrent hypoglycemia may promote and worsen seizures associated with hypoglycemia in diabetic children.