Thesis (Ph. D.)--Texas State University-San Marcos, 2006. / Vita. Appendices: leaves 343-357. Includes bibliographical references (leaves 358-370).

Theses (M.S.)--Marshall University, 2007. / Title from document title page. Includes abstract. Document formatted into pages: contains vii, 96 p. Includes vitae. Bibliography: p. 87-92.

Thesis (Ph. D.)--Texas State University-San Marcos, 2006. / Vita. Appendices: leaves 343-357. Includes bibliographical references (leaves 358-370).

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Thesis submitted in fulfillment of the requirements for the degree of Masters in Technology: Biomedical Sciences in the Faculty of Health and Wellness Sciences at the Cape Peninsula University of Technology 2015 / Background: The Mixed Ancestry population of South Africa has recently been reported to have a higher prevalence of type 2 diabetes (T2DM). However, the genetic risk factors that may contribute to the development of T2DM are currently unknown. We investigated the association of fat mass and obesity-associated gene (FTO), ectonucleotide pyrophosphatase/phosphodiesterase gene (ENPP1) and transcription factor 7-like 2 gene (TCF7L2) with T2DM risk in a community residing in Bellville South, Cape Town. Methods: Five hundred and sixty six participants (11.7% males) who consented to genetic analyses were genotyped for six single nucleotide polymorphisms (SNPs): ENPP1-rs997509 and -rs1044498, FTO-9941349 and -rs3751812, TCF7L2-rs12255372 and -rs7903146. The SNPs were genotyped using their corresponding Taqman genotyping assays, and validated by automated sequencing. Allele and genotype frequencies were determined and regression analyses was conducted to assess the association of the polymorphisms with T2DM and its related,traits. Results: Overall and in subgroups defined by diabetes and obesity statuses, there were present no significant differences in the distribution of alleles and genotypes, except for the polymorphisms observed in the FTO and ENPP1 genes. In logistic regression models adjusted for age, sex, body mass index (BMI) and insulin resistance, minor alleles of ENPP1-rs997509 and ENPP1-rs1044498 were associated with risk for T2DM respectively, 4.55 (1.06-19.49) (p=0.041) and 1.81 (1.09-2.98) (p=0.021) assuming a recessive genetic model. Furthermore, the FTO rs9941349 minor allele was associated with the prevalent T2DM under the log-additive model: 1.40 (1.00 to 1.96) (0.049). The TCF7L2 polymorphisms showed no evidence of association with T2DM and/or insulin sensitivity/resistance indicators. Conclusion: Our results demonstrate that ENPP1 and FTO polymorphisms may contribute to T2DM susceptibility in this population, confirming previous findings that insulin resistance may mediate the development of the disease in the Mixed Ancestry population group of South Africa.

The present study was designed to explore the mind-body connection within a psychosocial-cultural context. More specifically, the current investigator hoped to examine how various dimensions of the mind and body interact with psychosocial-environmental factors, which are significantly influenced by cultural processes and reference group membership A cross-sectional study was designed to examine the relationship between health beliefs and health behaviors in sample of 419 adults with Type II diabetes with a focus on the moderating effects of social support, emotional reactions, and experiences of unfair treatment. A self-report questionnaire comprised of 90-items obtained from previously established measures of health beliefs, psychosocial-cultural factors, and health behaviors was administered online via Qualtrics.com. Results of testing a series of measurement and structural models using confirmatory factor analysis (CFA) showed poor fit across all models specified. While these results indicated that the expanded Health Belief Model (eHBM) specified for this study did not adequately describe the diabetes-related thoughts, attitudes, and behaviors for the current sample of participants, findings may have provided preliminary evidence of a three-factor structure reflecting participants’ worries and concerns about their health & perceptions involving challenges or obstacles to successful behavior change, which could interfere with daily life. Although it is unclear whether these results were related to limitations in the measurement instruments and study design, or to differences in the nature of the constructs and the ways in which participants interpreted and responded to the scales, the overall findings of this study suggest a need for research that examines the equivalence of health belief and health behavior measures and greater empirical evidence to ensure that the theories and models used in health research are generalizable across groups of people with varying world-views, identities and lived experiences. Implications for the Health Belief Model (HBM) and ideas for future research are discussed.

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Abnormal regulation of growth hormone (GH) secretion has been reported in some patients with insulin-dependent diabetes (IDD). We compared the GH responses in 32 healthy subjects (age 25 ± 2 SE years) and in 23 IDD patients (28 ± 1.9 years old, diabetes duration 10.4 ± 2 years, and glycohemoglobin levels 9.3 ± 2.0%). During acute, severe hypoglycemia (glucose < 40 mg/dl), the mean GH levels were similar. When prolonged mild hypoglycemia was induced (58.0 ± 2.0 mg/dl in the controls and 54.0 ± 2.0 mg/dl in the IDD patients), the mean GH levels were similar, although the increase in GH was delayed in the latter group. During brief (30 min) exercise at 40-50% of VO2 max, GH rose comparably in both groups (IDD patients maintained euglycemia with basal insulin infusion). However, with more prolonged and intense exercise using a glucose clamp to maintain euglycemia, GH rose to 5.4 ± 2.2 ng/ml in controls and 26.4 ± 12.6 ng/ml in the diabetics (P < 0.05). When the combination of intense exercise and hypoglycemia (~ 55 mg/dl) was used, GH rose to a peak of 21.7 ± 2.7 ng/ml in the controls and to 33 ± 3.0 ng/ml in the diabetics (P = NS). Our data show that in insulin-infused IDD patients made euglycemic for these experiments: a) The GH response to acute, severe hypoglycemia was identical to that in the controls and the response to mild, prolonged hypoglycemia was delayed, but of similar magnitude compared with controls; b) Exercise-induced GH responses were observed in both groups, but exaggerated in the diabetics at a higher exercise intensity; c) Hypoglycemia during exercise produced an additive effect on GH secretion in the controls but not in the IDD patients. We conclude that the wide range of abnormal GH secretory responses in type I diabetes reflects a central, possibly hypothalamic, defect in GH regulation.

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No description available.