Thesis (Ph.D.)--University of Tasmania, 2005. / Includes 2 articles in back pocket. Includes bibliographical references.

Thesis (M.S.)--Auburn University, 2008. / Abstract. Vita. Includes bibliographical references.

Thesis (M.S.)--Auburn University, 2008. / Abstract. Vita. Includes bibliographical references (p. 100-116).

Thesis (M.A.)--University of North Carolina at Chapel Hill, 2004. / Includes bibliographical references (leaves 33-36). Also available online (PDF file) by a subscription to the set or by purchasing the individual file.

Thesis (M.A.)--University of North Carolina at Chapel Hill, 2004. / Includes bibliographical references (leaves 33-36).

Thesis (Ph. D.) University of Missouri-Columbia, 2006. / The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on July 31, 2007) Includes bibliographical references.

The entire thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file; a non-technical public abstract appears in the public.pdf file. Title from PDF of title page (University of Missouri--Columbia, viewed on November 19, 2009). Thesis advisor: Dr. Thyfault. Includes bibliographical references.

Introduction: Metabolic syndrome and depression are considered to be important risk factors for the development of cardiovascular diseases. The prevalence of metabolic syndrome is estimated to be around 25% of the adult population in industrialized countries, including the population of Czech Republic. The prevalence of depression is estimated to be around 15% of the same adult population. It is not clear yet on the base of poor literature, which is so far available, whether there is a causal relationship between these factors or not. Objective: To try to find a relationship between metabolic syndrome and depression in a population sample using clinical and metabolic parameters. Methods: The prevalence of depressivity or other psychopathologies was evaluated with the use of self-report questionnaires in a randomly selected population sample of 259 people living in Pilsen. The questionnaires were mailed to the subjects. Those of them who responded were invited to the examination of anthropometric and laboratory parameters defining the metabolic syndrome and to the examination of some other parameters. The occurrence of risk factors of the metabolic syndrome of insulin resistance and the relationship between depression and metabolic syndrome was investigated. Metabolic syndrome of insulin resistance...

M.Tech. (Homoeopathy) / Insulin resistance is defined as the impaired ability of plasma insulin to facilitate peripheral glucose disposal, suppress hepatic gluconeogenesis and inhibit very low density lipoprotein (VLDL) output (Caceres et al., 2008). Insulin resistance is not a disease, but rather a feature and attribute of the Metabolic Syndrome, which is associated with a high risk of developing type two diabetes mellitus and cardiovascular disease (Brewer, 2005). Insulin resistance (IR) is globally regarded as the common and fundamental aetiological factor of the various components of the Metabolic Syndrome namely abdominal obesity, dyslipidaemia, insulin resistance and hypertension (Zimmet, 1991; Haffner et al., 1992 Stern, 1997; Beck Nielson & Groop, 1994; Tsai et al., 2012). Diabetes mellitus type 2 is a rapidly growing worldwide epidemic, but only diagnosed once the underlying metabolic abnormalities have caused damage. The fact that many recently diagnosed diabetic patients already suffer from so called “late complications of diabetes” indicates that the pre-diabetic condition is harmful to health and needs to be addressed promptly to slow down or avoid the progression to diabetes mellitus type 2 (Beck Nielson & Groop, 1994; Brewer, 2005; Tsai et al., 2012). Treatment of insulin resistance proves very difficult as dietary and lifestyle choices play an integral role in the development, treatment and management of insulin resistance; and insulin resistant patients also seem resistant to changing their behaviour (Brewer, 2005). Current conventional treatment options are limited in efficacy and may be associated with significant side-effects (Brewer, 2005; Snyman, 2009; Neal, 2003), while coherent studies on combination complementary forms of treatment are lacking (Chen et al., 2003; Guan et al., 2000; Hull, 2008; Verma et al., 1998; Winston & Kuhn, 2007; Ye et al., 2001). This study aimed to determine the efficacy of the herbal and nutritional formulation Glucostate™ in FoodState® form, on the HOMA index of insulin resistant patients. This was a collaborative randomized double-blind and double-dummy placebo controlled quantitative research study that included 40 participants. Due to the inherent nature of associated race, age and gender bias, participants were matched according to these criteria and randomly allocated to either an experimental or control group (Appendix C). The placebo group was shared between two collaborative studies. Participants volunteered to participate in the study, were between the ages of 20-45 years and consented to the procedures of the study. Participants in the treatment group received Glucostate™ tablets and placebo drops and the participants in the placebo group received placebo tablets and placebo drops. The research study was conducted over a period of 16 weeks per participant at the University of Johannesburg Health Training Centre, Doornfontein Campus. Participants were asked to maintain their original lifestyle and diet and continue as is normal for them, as alterations in weight have an effect on insulin levels. Participants were screened using blood pressure, abdominal girth, height, weight and Body Mass Index (BMI); these measurements were repeated at weeks 4, 8, 12 and 16. Fasting blood tests consisting of a lipogram, fasting glucose and fasting insulin level were done prior to and at the conclusion of the study. The Homeostasis Model Assessment (HOMA) index was calculated from the fasting insulin and glucose values. Results acquired from the research study were statistically analyzed by Statkon at the University of Johannesburg by means of descriptive statistics, parametric and non-parametric tests. The only parameters which showed statistically significant improvement for the Glucostate™ group and not the placebo group were systolic blood pressure (SBP) (p=0.004) and diastolic blood pressure (DBP) (p=0.050). There was no statistically significant change in any of the other parameters when compared to placebo. This research study determined that Glucostate™ was not effective in reducing insulin resistance and the parameters directly associated with its measurement especially when compared to the effects of placebo.

Background and objective: Childhood obesity is a serious global health problem and it is associated with insulin resistance and significantly increased risk for development of type 2 diabetes and cardiovascular disease. Metformin reduces the risk of developing T2D in adult patients with obesity and insulin resistance. However there is limited and inconclusive data in obese non diabetic children and adolescents. The objective of the Metformin in Obese Children and Adolescents (MOCA trial) was to assess the effect of metformin on body composition, metabolic risk factors and adipokines. Design and methods: The MOCA trial was a six month multi-centre randomized, double-blind placebo-controlled trial of metformin (1.5g daily) in children and adolescents (8-18 years) with insulin resistance and/or impaired glucose tolerance. Auxology, blood pressure measurement and fasting blood tests (insulin, glucose, fasting lipids, ALT, bilirubin, CRP, lactate, resistin, adiponectin, leptin) were performed at baseline, three and six months. A prolonged oral glucose tolerance test was performed at baseline and after six months. Measures of insulin resistance/sensitivity were calculated including HOMA-IR and the adiponectin: leptin (A/L) ratio. Results: 151 obese children participated in the trial (metformin:77, placebo:78). 102 (67.5%) female, 99 (65.6%) post-pubertal, 115 (76.2%) White British and 36 (23.8%) British Asian or Afro-Caribbean. Mean age of participants was 13.7 ±2.3 year and mean BMI-SDS 3.4 (0.5). In regression analysis, controlling for baseline values, sex, ethnicity and pubertal status, metformin had a greater treatment effect over placebo for BMI at three months, that was sustained at six months (-0.25 kg/m2, p=0.01, 95% CI 0.29 to 1.86) and BMI-SDS (-0.1, p=0.01, 95% CI 0.02 to 0.19). Fasting glucose reduced (-0.03 mmol/l, p=0.03) and A/L ratio increased at three months (+0.04, p=0.03), but the improvements were lost at six months. The other measures of insulin sensitivity, metabolic risk factors and concentrations of adipokines did not change with metformin treatment. Conclusions: Metformin therapy for obese children with abnormal insulin glucose status is safe, well tolerated and has a small beneficial treatment effect over placebo for BMI, BMI-SDS, fasting glucose and A/L ratio at three months, with the changes in body composition sustained at six months. A three month course of metformin should be considered by Paediatricians to halt the inexorable rise in BMI-SDS in these children, improve insulin glucose status and act as catalyst and support for more radical change in lifestyle in the individual. Trial register number: ISRCTN 19517475.