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This PhD thesis describes a systematic process of developing an evidence-based and theory coherent behaviour change intervention for obese adults with additional risk factors. A systematic review assessed the effects of behavioural interventions on changes in behaviour, weight, and cardiovascular disease risk factors in randomised controlled trials sampling obese adults with additional risk factors for morbidity. Small-to-modest improvements were detected in all variables with significant heterogeneity within outcomes. Moderator analyses of programme and delivery components on weight and behaviour revealed various intervention components associated with more successful intervention including. These components included self-monitoring, provision of instructions, and relapse prevention to change dietary behaviour and prompting practice for physical activity behaviour change. These components subsequently informed the development and design of an evidence-based and theory coherent behaviour change intervention. Evidence on modes of delivery, behaviour change techniques and theory were integrated into an intervention package. An open pilot study testing and optimising acceptability and feasibility of the content, procedures and materials of the development intervention was conducted. The intervention was delivered to obese participants in a clinic setting, with facilitator and participant feedback collected during and after intervention delivery. The open pilot evidenced the intervention to be feasible for delivery and highly acceptable to a sample of at-risk participants in great need of behavioural change. The work undertaken as part of this thesis provides a practical example how to systematically develop an evidence-based and theory coherent behaviour change intervention.

This study was conducted to test the hypothesis that dietary arginine supplementation reduces fat mass in diet-induced obese rats. Male Sprague-Dawley rats were fed either low- or high-fat diets for 15 wks (16 rats/diet). Thereafter, lean or obese rats continued to be fed their same respective diets and received drinking water containing either 1.51% L-arginine-HCl or 2.55% alanine (isonitrogenous control) (n=8/treatment group). Twelve weeks after the initiation of the arginine treatment, rats were euthanized to obtain tissues for biochemical analyses. Results were statistically analyzed as a 2x2 factorial experimental design using ANOVA. High-fat diet increased the mass of white adipose tissues at different anatomical locations by 49-96% compared to the low-fat diet. Concentrations of serum cholesterol as well as lipids in skeletal muscle and liver were higher in obese rats than in lean rats. L-Arginine supplementation reduced white adipose tissue mass by 20-40% while increasing brown adipose tissue mass by 15-20%. In addition, arginine treatment decreased adipocyte size, serum concentrations of glucose, triglycerides and leptin, improved glucose tolerance, and enhanced glucose and oleic acid oxidation in skeletal muscles. The mRNA levels for hepatic fatty acid synthase and stearoyl-CoA desaturase were reduced, but mRNA levels for hepatic AMP-activated protein kinase (AMPK), PPAR coactivator-1 and carnitine palmitoyltransferase I (CPT-I) as well as muscle CPT-I were increased in response to the arginine treatment. Subsequent experiments were conducted with cell models to define the direct effects of arginine on energy-substrate metabolism in insulin-sensitive cells. In BNL CL.2 mouse hepatocytes, C2C12 mouse myotubes and 3T3-L1 mouse adipocytes, increasing extracellular concentrations of arginine from 0 to 400 µM increased AMPK expression as well as glucose and oleic acid oxidation. Inhibition of nitric oxide synthesis moderately attenuated the arginine-stimulated increases of substrate oxidation as well as AMPK and ACC phosphorylation in BNL CL.2 cells, but had no effect in C2C12 and 3T3-L1 cells. Collectively, these results suggest that arginine increases AMPK expression and energy-substrate oxidation in a cell-specific manner, thereby reducing fat mass in diet-induced obese rats. The findings have important implications for treating obesity in humans and companion animals as well as decreasing fat deposition in livestock species.

Thesis--PlanB (M.S.)--University of Wisconsin--Stout, 2002. / Includes bibliographical references.

Thesis--University of Denver. / eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Background Globally, epidemics of obesity and influenza are always two major public health issues that require immediate actions for human. After the outbreak of pandemic influenza A (H1N1) in 2009, the relationship between obesity and influenza was widely recognized due to severe illness and reported death with obesity among infected cases. We still doubted whether obesity is a risk factor for influenza infection or not. So I conducted this systemic review to explore the association between obesity and influenza A morbidity or mortality. Method PubMed, Google scholar, and HKU library were searched using a prepared strategy for all items in English up to 31 July 2014. Search strategy, exclusion and inclusion criteria, assessment of quality, as well as data analysis were established for screening all relevant publications. Findings Through careful screening, 17 relevant studies were adopted into this review. There were 9 case control studies of all observational studies. Obesity and morbid obesity in influenza A infected adults (below 60 years old) could be regarded as a risk factor for hospitalization and severe sickness. Morbid obesity would be related with higher risk for mortality and ICU admission. Conclusion From my review, there was a strong association between obesity and influenza A infection had been confirmed. However, we need to carry out further research to explore the details of impacts. Obese people, as the high-risk population, should take vaccine during influenza season to protect themselves effectively. / published_or_final_version / Public Health / Master / Master of Public Health

Obesity is a major epidemic and an independent risk factor for heart disease. Food derived compounds such as resveratrol has been reported to have strong medicinal properties and shown potential in preventing and reversing heart diseases. This study investigated the cardioprotective properties of resveratrol in an animal model of diet induced obesity and possible cellular mechanisms. Obese prone (OP) and obese resistant (OR) rats were fed with high fat diet while, sprague dawley (SD) rats that served as control were fed with normal lab chow for a total of 17 weeks. During the last 5 weeks of study, treatment group received resveratrol daily by oral gavage at a dosage of 2.5 mg/kg body weight. Treatment with resveratrol significantly improved cardiac isovolumic relaxation time (IVRT), thiobarbituric acid reactive substance (TBARS), tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), triglycerides, glucose, low density lipoprotein and increased insulin in OP rats and TNF-α, glucose and leptin in OR rats. Cardiac calcium handling proteins such as sarcoendoplasmic reticulum Ca2+-ATPase2a (SERCA2a), phospholamban (PLB) and phosphorylated PLBthr17 and PLBser16 were unchanged in all the groups. Excess circulating lipids cause cellular dysfunction in major organs. Adult rat cardiomyocytes were incubated for 24 hours with different doses (10, 100 and 200µM) of palmitic acid (PA). One group cardiomyocytes were pretreated with resveratrol for 45minutes prior to addition of PA. Incubation with 200µM PA significantly increased the number of round shaped cardiomyocytes and apoptosis and resveratrol treatment prevented these changes. Cardiomyocytes contractility measurement showed 200µM PA resulted in reduced rate of relaxation and resveratrol prevented this reduction. Western blot analysis showed that the PA induced a 17% decrease in SERCA2a expression and SERCA2A:PLB ratio was preserved with resveratrol treatment. The change in SERCA2a with PA and resveratrol exposure was statistically not significant. In conclusion, resveratrol treatment reversed cardiac abnormalities in OP rats, but not in OR rats. Resveratrol treatment prevented PA induced contractile abnormality in adult cardiomyocytes. Importantly, this study showed that resveratrol can act directly on cardiomyocytes and protect against damage from exposure to high levels of lipids. / February 2015

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