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Using the Limited Capacity Model of hostility (Walters & Harrison, 2006; Williamson & Harrison, 2005; Williamson, Harrison, & Walters, 2007) as a guide, the stress response of individuals with a variable and dysregulated fuel supply to their brain (diabetes) was examined subsequent to lateralized fluency-stress. This theoretical "capacity" model of hostility was applied to a relatively unknown population of high hostile-diabetics. Given the associations between hostility and diabetes, it was argued that a very robust stress response would be evident, as measured as by peripheral glucose and QEEG magnitudes, as a result of modest regulatory capacity subsequent to right frontal lobe stress. Moreover, it was expected that high hostile-diabetics would show diminished performance on neuropsychological indicants of right frontal functions. / Ph. D.

Glucose and lipid metabolism are dysregulated in obese horses. Altered glucose metabolism is evidenced by the development of insulin resistance and increased fasting plasma insulin concentrations (hyperinsulinemia) while altered lipid metabolism is evidenced by increased plasma lipid concentrations. Obesity in horses also increases the risk of the painful hoof disease, laminitis. Three experiments were performed to investigate the regulation of nutrient metabolism in skeletal muscle and adipose tissue of lean, healthy horses. Adipose tissue was found to be the primary lipogenic tissue of horses, with acetate being the primary lipogenic substrate. Secondly, ten, lean horses were used to investigate the effects of acute hyperinsulinemia on nutrient metabolism. Increasing plasma insulin concentrations to >1,000 mIU/L for six hours decreased transcript abundance of glucose transporters and the insulin receptor in adipose tissue, and decreased protein abundance of the insulin receptor in skeletal muscle, potentially indicating that hyperinsulinemia potentiates insulin resistance. Insulin infusion also reduced mRNA abundance of lipid transporters in adipose tissue while increasing them in skeletal muscle. The final experiment investigated the influence of the insulin-sensitizing drug, pioglitazone, and lipopolysaccharide, on nutrient metabolism in skeletal muscle and adipose tissue, and their association with insulin sensitivity. Pioglitazone treatment did not increase insulin sensitivity; however it did increase skeletal muscle transcript abundance of the insulin receptor and the non-insulin sensitive glucose transporter and adipose tissue protein abundance of the insulin-sensitive glucose transporter (GLUT4). Lipopolysaccharide decreased insulin sensitivity regardless of pioglitazone pre-treatment, which was associated with decreased transcript abundance of GLUT4 in skeletal muscle and adipose tissue of untreated horses, but not adipose tissue of pioglitazone treated horses. / Ph. D.

The objective of the study was to investigate and characterize the effects of a continuous rate infusion of dextrose or dextrose and insulin on glucose and insulin dynamics in both healthy and endotoxin-exposed horses. Administration of a low dose of endotoxin has been used in horses to mimic the clinicopathologic changes seen in endotoxemia, including the development of an inflammatory response. Our hypothesis was that a continuous rate infusion of insulin at a rate of 0.07 IU/kg/hr would prevent the development of hyperglycemia induced by administration of dextrose in both healthy and endotoxin-exposed horses. Nine healthy adult horses were used in the study. In Phase 1 of the experiment, horses received a saline infusion or a dextrose infusion in a balanced crossover design. In Phase 2 of the experiment, horses received a dextrose and insulin infusion, both prior to and after receiving a low dose of endotoxin (no LPS group and LPS group respectively) in a balanced crossover design. Blood samples were collected at regular intervals throughout both phases for measurement of plasma glucose and insulin concentrations. Infusion of dextrose alone resulted in hyperglycemia for nearly the entire study period. Insulin concentration was also increased in comparison to the saline infusion. When comparing the dextrose treatment group to the combined dextrose and insulin treatment group (no LPS group), the insulin levels were significantly greater over time in the latter group and resulted in maintenance of euglycemia. When comparing the no LPS group to the LPS group, both the glucose and insulin concentrations were higher in the LPS group but euglycemia was still achieved. These results serve to validate the dose of insulin used in this study (0.07 IU/kg/hr) in regards to effective prevention of hyperglycemia when administered concurrently with a dextrose infusion. Hyperglycemia was prevented in both healthy and endotoxin-exposed horses. In addition, the dose of insulin used was demonstrated to be safe, as hypoglycemia did not occur in any of the horses. / Master of Science

Yeung Ho Lam. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2006. / Includes bibliographical references (leaves 93-107). / Abstracts in English and Chinese. / Thesis Committee --- p.i / Abstract --- p.ii / 摘要 --- p.iv / Acknowledgments --- p.v / Table of Contents --- p.vi / List of Abbreviations --- p.x / List of Figures --- p.xiii / List of Tables --- p.xv / Chapter CHAPTER 1 --- INTRODUCTION --- p.1 / Chapter 1.1 --- Glucose Transport through the Blood Brain Barrier --- p.1 / Chapter 1.2 --- Roles of Astrocytes in the Brain --- p.4 / Chapter 1.3 --- Glucose Metabolism in Astrocytes --- p.8 / Chapter 1.4 --- Diseases Associated with Reduced Glucose Transport --- p.10 / Chapter 1.5 --- Extracellular Accumulation of Glutamate as a Cause for Epilepsy --- p.13 / Chapter 1.6 --- Regulations of Astrocyte-mediated Glutamate Uptake --- p.17 / Chapter 1.7 --- Aim and Hypothesis of the Project --- p.22 / Chapter CHAPTER 2 --- MATERIALS AND METHODS --- p.24 / Chapter 2.1 --- Materials --- p.24 / Chapter 2.1.1 --- Primary Rat Astrocytes --- p.24 / Chapter 2.1.2 --- Cell Culture Materials --- p.24 / Chapter 2.1.3 --- Chemicals --- p.26 / Chapter 2.1.4 --- Reagents for the Determination of Gene Expressions --- p.26 / Chapter 2.1.5 --- Reagents for the Determination of Protein Expressions --- p.29 / Chapter 2.1.6 --- Reagents for Functional Assays --- p.33 / Chapter 2.1.6.1 --- Reagents for Enzyme-Linked Immunosorbent Assay (ELISA) of IL-6 --- p.33 / Chapter 2.1.6.2 --- Reagents for Glutamate Uptake Assay --- p.33 / Chapter 2.1.6.3 --- Reagents for Extracellular Glutamate Determination Assay --- p.33 / Chapter 2.1.6.4 --- Reagents for Glucose Uptake Assay --- p.34 / Chapter 2.1.6.5 --- Reagents for MTT Assay --- p.34 / Chapter 2.1.6.6 --- Reagents for GFAP Immunostaining --- p.35 / Chapter 2.2 --- Methods --- p.36 / Chapter 2.2.1 --- Preparation of Primary Astrocytes --- p.36 / Chapter 2.2.2 --- Determination of Gene Expressions by Reverse Transcription-Polymersase Chain Reaction (RT-PCR) --- p.37 / Chapter 2.2.3 --- Determination of Protein Expressions by Western Blotting --- p.40 / Chapter 2.2.4 --- ELISA --- p.43 / Chapter 2.2.5 --- Glutamate Uptake Assay --- p.44 / Chapter 2.2.6 --- Extracellular Glutamate Determination Assay --- p.44 / Chapter 2.2.7 --- Glucose Uptake --- p.45 / Chapter 2.2.8 --- MTT Assay --- p.46 / Chapter 2.2.9 --- GFAP Immunostaining --- p.46 / Chapter 2.2.10 --- Band Intensity Quantification --- p.47 / Chapter 2.2.11 --- Statistical Analysis --- p.47 / Chapter CHAPTER 3 --- RESULTS --- p.49 / Chapter 3.1 --- Preparation of Primary Astrocyte Culture --- p.49 / Chapter 3.2 --- Effects of Glucose Deficiency on Astrocyte-mediated Glutamate Uptake --- p.51 / Chapter 3.2.1 --- Effects of Glucose Deficiency on the Expressions of Glutamate Transporters --- p.51 / Chapter 3.2.2 --- Effects of Glucose Deficiency on Glutamate Uptake in Primary Astrocytes --- p.56 / Chapter 3.3 --- Astrocytic Glucose Transport under Glucose Deficiency --- p.61 / Chapter 3.3.1 --- Effects of Glucose Deficiency on the Expressions and Secretion of Inflammatory Cytokines --- p.64 / Chapter 3.3.2 --- Effects of Exogenous Interleukin-6 on Energy Availability in Primary Astrocytes upon Glucose Deficiency --- p.70 / Chapter 3.4 --- Signaling Mechanism Mediating the Astrocytic Responses under Glucose Deficiency --- p.74 / Chapter 3.4.1 --- Effects of Glucose Deficiency on the Expressions of Total and Phosphorylated ERK1/2 in Primary Astrocytes --- p.74 / Chapter CHAPTER 4 --- DISCUSSIONS AND CONCLUSIONS --- p.81 / Chapter 4.1 --- Role of Astrocytes in Preventing Glutamate Excitotoxicity under Glucose Deficiency --- p.81 / Chapter 4.1.1 --- Neonatal Astrocytes as the Cell Model for Chronic Glucose Deficiency --- p.81 / Chapter 4.1.2 --- Effects of Glucose Deficiency on the Expressions of Glutamate Transporters and Glutamate Uptake --- p.83 / Chapter 4.1.3 --- Cytokines: Mediators for Energy Production in Astrocytes --- p.85 / Chapter 4.1.4 --- Summary of the Roles of Astrocyets under Prolonged Glucose Deficiency --- p.88 / Chapter 4.2 --- Establishment of an in vitro GlutlDS model --- p.89 / Chapter 4.3 --- Future Directions of the Project --- p.90 / Chapter 4.4 --- Conclusion --- p.92 / REFERENCES --- p.93 / APPENDIX --- p.108

The purpose of this study was to analyze the experiences of self-monitoring of blood glucose (SMBG) usage of adults with type 2 diabetes mellitus (T2DM) who are not using insulin. The sample consisted of 11 women and 8 men who were Caucasian Americans, 38 to 79 years of age. Data were analyzed using the grounded theory method including open and axial coding and the constant comparative method. The theory of "SMBG as a Cue in T2DM Self-Care" emerged from the data and is composed of four categories (a) Engaging, (b) Checking, (c) Responding, and (d) Establishing a Pattern. Engaging marks the beginning of SMBG. Participants began on the recommendation of their physician and monitored between 2-6 times a day. Participants monitored because of curiosity and over time reduced or kept their initial frequency. Checking occurs when the blood glucose is obtained. Two subcategories emerged: Evaluating and Validating. The main items participants evaluated or validated were the effects of foods in relation to blood glucose levels. Responding involves reacting to SMBG. Two subcategories emerged: Taking Action and Experiencing Emotion. Most actions involved changing foods consumed. Participants described feeling conflicted and "being bad" when not following through with an action. Emotions such as blame and fear were experienced when blood glucose levels were higher than normal, while happiness was experienced with normal levels. Establishing a Pattern occurs when participants decide on how often to monitor. Two subcategories emerged: Using Regularly and Using Sporadically. The pattern developed was based on obtaining "normal" blood glucose patterns or on the absence of ill symptoms of T2DM. Healthcare provider disinterest in SMBG and fingertip pain contributed to a decreased monitoring frequency. Participants described cyclical, iterative episodes of Checking, Responding, and varying their established patterns throughout their experiences with monitoring. Participants discussed the value and struggles of SMBG in a T2DM self-care regimen. The theory of SMBG as a Cue in T2DM Self-Care could be used to guide the development of effective intervention strategies to help individuals with T2DM achieve blood glucose control which, in turn, leads to avoidance of ill symptoms and complications of T2DM.

Thesis (Ph.D.)--Indiana University, 2009. / Title from screen (viewed on December 9, 2009). Department of Biochemistry and Molecular Biology, Indiana University-Purdue University Indianapolis (IUPUI). Advisor(s): Jeffrey S. Elmendorf, Peter J. Roach, Joseph T. Brozinick, Michael S. Sturek, Robert V. Considine. Includes vitae. Includes bibliographical references (leaves 97-124).

Diss. (sammanfattning) Stockholm : Karol. inst., 2003. / Härtill 5 uppsatser.

INTRODUCTION: Type 1 diabetes (T1D) is a lifelong disease that requires regular injection of insulin and blood glucose (BG) monitoring. Many diabetes technologies have been created to assist in the management of T1D, including insulin pumps and Continuous Glucose Monitoring (CGM). These systems have been shown to decrease treatment distress and improve glycemic control. However, the uptake of these systems is low due to both cost and other barriers such as discomfort of wear or psychosocial aspects. METHODS: A survey was administered to clinicians of people with diabetes to better understand their perception of patient related barriers to device use. This analysis compares two clusters of clinicians, named "Cautious" and "Ready" based on their readiness to promote CGM use in their patients. Both have positive attitudes towards technology, but the Cautious cluster perceives much higher barriers to device use in their patients than the Ready cluster. In this analysis, the individual barriers, prerequisites to CGM use, confidence in addressing barriers, and clinic staff resources are compared between clusters using independent means t-tests and Pearson chi-square analyses. RESULTS: Results indicate that the confidence in addressing the clinician-reported number 1 rated barrier to CGM use was significantly lower in the Cautious cluster. Also, most individual barriers were perceived significantly more heavily by clinicians in the Cautious cluster. No significant difference was found in prerequisites to CGM use or clinic staff resources between the clusters. DISCUSSION: Because no differences were found in clinician reported prerequisites to CGM use between clusters, it does not seem that the clinicians in the Cautious cluster expect more from their patients before using this technology. One possible explanation would be a clinical deficiency. However, since there was no difference in clinic staff resources, it is unlikely that the availability of these resources contributes to the increased perceived barriers. Thus, the problem may lie in the clinician themselves. One possible explanation for the increased perceived barriers by the Cautious cluster is their lack of confidence in addressing barriers. Our results show that the Cautious cluster is significantly less confident in addressing the #1 barrier their patients face to CGM use, which is most commonly listed as cost-related barriers such as cost of the device or insurance status. One possible solution to this lack of confidence in clinicians is increased education on ways to address and coach patients on cost-related barriers.

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