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abstract: Obesity in Hispanic youth has reached alarmingly high levels, increasing the risk of type 2 diabetes, hyperlipidemia, hypertension, and cardiovascular disease. In Mexican American children ages 6-11 years, 41.7% are overweight and obese, 24.7% are obese and 19.6% have a Body Mass Index (BMI) greater than the 97th percentile. While personal, behavioral, and environmental factors contribute to these high rates, emerging literature suggests acculturation, self-efficacy and social support are key influences. The one-group, pre- and post-test, quasi-experimental design used a community-based participatory research (CBPR) method to test the feasibility, acceptability, and preliminary efficacy of the 8-week intervention. Social Cognitive Theory (SCT) was used to guide the design. Measurements included an analysis of recruitment, retention, participant satisfaction, observation of intervention sessions, paired t-tests, effect sizes, and bivariate correlations between study variables (acculturation, nutrition and physical activity [PA] knowledge, attitude and behaviors, perceived confidence and social support) and outcome variables (BMI z-score, waist circumference and BP percentile) Findings showed the SSLN program was feasible and acceptable. Participants (n = 16) reported that the curriculum was fun and they learned about nutrition and PA. The retention rate was 94%. The preliminary effects on adolescent nutrition and PA behaviors showed mixed results with small-to-medium effect sizes for nutrition knowledge and attitude, PA and sedentary behavior. Correlation analysis among acculturation and study variables was not significant. Positive associations were found between perceived confidence in eating and nutrition attitude (r = .61, p < .05) and nutrition behavior (r = .62, p < .05), perceived confidence in exercise and nutrition behavior (r = .66, p < .05), social support from family for exercise and PA behavior (r = .67, p < .01) and social support from friends for exercise and PA behavior (r = .56, p < .05). These findings suggest a culturally specific healthy eating and activity program for adolescents was feasible and acceptable and warrants further investigation, since it may fill a gap in existing obesity programs designed for Hispanic youth. The positive correlations suggest further testing of the theoretical model. / Dissertation/Thesis / Ph.D. Nursing and Healthcare Innovation 2011

Adipose tissue plays an essential role in the regulation of many metabolic processes. Excess caloric intake and decreased energy expenditure cause adipocyte hypertrophy and hyperplasia, leading to inflammation of the adipose tissue, which contributes to obesity. Recent data link the Receptor for Advanced Glycation End-products (RAGE) to high fat diet (HFD)-induced obesity and subsequent metabolic dysfunction, but its function is incompletely understood. On HFD, the concentration of RAGE ligands, such as carboxy methyl lysine (CML) - advanced glycation end-products (AGE) epitopes, S100 calcium binding protein B (S100b), and high mobility group box 1 (HMGB1) increases, activating RAGE and resulting in inflammation. However, deletion of RAGE protected against the HFD-induced obesity and resulted in increased overall energy expenditure. In this study, we tested the hypothesis that the protective mechanism of RAGE deletion is due, in part, to browning which involves inducing brown adipose tissue (BAT)-like properties in white adipose tissue (WAT). The expression of uncoupling protein 1 (UCP1), which is usually only expressed in BAT, is increased in the WAT of RAGE knockout (RKO) mice. This effect was reproduced in vitro, by silencing the Ager gene in the adipocyte cell line C3H10T1/2. We propose that RAGE affects adipocyte phenotype by downregulating the expression of browning genes such as UCP1, and therefore is a key determinant of energy expenditure and adiposity. Thus, RAGE antagonism may promote BAT phenotype and function in WAT, reducing adiposity, which may have potential therapeutic implications for treating obesity. / 2017-03-31T00:00:00Z

BACKGROUND: Poor self-regulation during preschool and early school age years is associated with rapid weight gain. However, the association between self-regulatory capacities in infancy and weight status in early childhood has not been well studied. Objective: Examine prospective associations between infant self-regulation and body mass index (BMI) in early childhood. We hypothesized that infants exhibiting less optimal self-regulation would be at greater risk of obesity at 3–5 years of life. METHODS: We used data from 5750 children in the Early Childhood Longitudinal Study-Birth Cohort (ECLS-B), excluding premature infants and infants small or large for gestational age. Our primary predictor was infant self-regulation measured at age 9 months by parent completion of the Infant Toddler Symptom Checklist (ITSC). We defined child obesity at preschool and kindergarten age (approximately 4 years and 5–6 years respectively) as a body mass index (BMI) ≥ 95th percentile for age and sex by US Centers for Disease Control growth charts. We created logistic regression models comparing risk of obesity at preschool and kindergarten age in infants with ITSC scores ≥ 6 to infants with scores < 6, controlling for covariates. RESULTS: Twenty-one percent of children with ITSC scores ≥ 6 at 9 months were obese at preschool age compared to 16% of children with lower ITSC scores. At kindergarten age this difference decreased to 18% vs. 16% respectively. After adjusting for covariates, infants with ITSC scores ≥ 6 had 32% increased odds of being obese at preschool age (aOR 1.32; 95% CI: 1.03, 1.70) though this association decreased at kindergarten age (aOR 1.07; 95% CI: 0.79, 1.45). CONCLUSIONS: Poor infant self-regulation at 9 months is associated with an increased risk of obesity at preschool entry but not at kindergarten entry. Helping parents manage and respond to children’s self-regulation difficulties prior to preschool age may serve as a focal point for future interventions. / 2016-12-01T00:00:00Z

The global rise in the prevalence of obesity has been labeled a pandemic. The increasing rates of overweight and obese persons across the world is discerning, as obesity is a risk factor for many life-threatening and debilitating diseases including type two diabetes mellitus (T2DM), a disease that decreases insulin sensitivity of skeletal muscle, adipose tissue and liver, and insulin secretion in pancreatic beta cells. Despite its pervasiveness, the mechanism by which obesity causes T2DM remains elusive. Adipose tissue is known to contribute to whole body glucose metabolism and as a result has been implicated in T2DM. Obesity causes changes in the physiology of adipose tissue, including hypertrophy of adipocytes, rendering them stressed and dysfunctional. The result is an increase in free fatty acids in the blood, due to increased lipolysis and decreased triglyceride storage. Free fatty acids have been shown to cause insulin resistance in insulin sensitive tissues. It has also been observed that in some patients, obesity results in inflammation of adipose tissue. As adipocytes enlarge, they not only secrete increasing amounts of free fatty acids, they also secrete chemoattractant proteins like MCP-1, which attract macrophages. These macrophages secrete inflammatory cytokines such as Tumor Necrosis Factor- alpha, Interleukin-1beta and Interleukin-6, among others, which have been shown to alter adipose tissue metabolism by increasing lipolysis and decreasing triglyceride storage. In addition, inflammatory cytokines have been suspected to play a role in insulin resistance, although the exact mechanisms remain elusive. The present study explored the possibility that Interleukin-1beta and Interleukin-6 affect insulin signaling in human adipocytes by increasing lipolysis, thus increasing free fatty acids in the blood. Recent studies have emphasized the role of fat specific protein 27 (FSP27) in the regulation of lipolysis in adipocytes whereby, FSP27 controls lipolysis by regulating the lipolytic capacity as well as transcription of the primary lipase ATGL. In the present study we used FSP27 as a tool to investigate if managing lipolysis could protect human adipocytes from the impairment of insulin signaling caused by the presence of inflammatory cytokines. We found that Interleukin-1beta and Interleukin-6 increase lipolysis in human adipocytes by depression of endogenous FSP27 protein levels and that the rate of lipolysis can be rescued by adenoviral expression of FSP27. In addition, we found that interleukin-1beta decreased insulin signaling by decreasing phosphorylation of AKT and that adenoviral expression of FSP27 has a protective effect over Interleukin-1beta - induced impairment of insulin signaling in human adipocytes. Our experiments regarding the effect of Interleukin-6 on insulin signaling were inconclusive and need further experimentation. These results suggest that the inflammatory cytokine Interleukin-1beta indirectly suppresses insulin signaling, by increasing lipolysis and that maintenance of FSP27 protein levels in obese patients could prevent patients from developing insulin resistance and T2DM.

Thesis (M.A.) / It is well known obesity rates have climbed steadily since the 1960s. The result is an increasing burden on healthcare in the world and especially, the United States. Those costs are not simply financial, but obesity, defined as a chronic disease of excess fat, has many comorbid diseases associated with it, along with decreased productivity and happiness. Trends in depression of the past few decades mirror those of obesity, as depression is more prevalent than ever. Likewise, depression places a heavy burden on the healthcare infrastructure. Many different researchers have sought a link between these two chronic diseases, and it is the goal of this paper to review this evidence. Investigators have framed the potential relationship in many different ways, including a sociological argument, with either obesity or depression predisposing the other, being elements in a shared inflammatory pathway, CNS pathway, HPA axis, and serotonin pathway. More studies are needed to conclude there is a definitive link between obesity and depression, but because of the massive toll both conditions take on the individual and society, it is well worth the investment. Perhaps, the success of obesity treatments that address depression, diminished self-worth and self-esteem provide some promise, and they also provide a new avenue to study this relationship. In identifying the comprehensive approaches to obesity that are most effective, researchers may be able to work backwards, identifying all the elements being touch upon by the treatment. / 2031-01-01

Obesity is the most common antenatal comorbidity, affecting one in five of the antenatal population in the UK. It is associated with adverse outcomes for mother and baby in both the short and long term. Increasing data suggest that maternal obesity may programme offspring later life obesity and premature mortality, with high birth weight being a marker for increased risk. The mechanism by which maternal obesity causes excessive neonatal birth weight is incompletely understood but considerable evidence implicates insulin resistance and/or hyperglycaemia. There are currently no effective interventions to mitigate the effects of obesity during pregnancy. In this thesis, we present the findings from a randomised, double blind, placebo controlled trial designed to examine the efficacy of metformin, an insulin-sensitising agent, in obese pregnant women. The aim of the trial was to determine whether giving metformin to obese pregnant women from between 12 and 16 weeks’ gestation until birth, would improve maternal and fetal outcomes. The primary outcome measure was birth weight of the baby, using this as a surrogate marker for the future life risk of the child developing obesity. Nested within this large clinical trial were a series of mechanistic sub-studies. To examine the effect of metformin on maternal insulin resistance at 36 weeks’ gestation, we used the hyperinsulinaemic euglycaemic clamp with concomitant use of stable isotope tracers. This enabled us to characterise in greater detail insulin sensitivity, endogenous glucose production and lipolysis. To determine the effect of metformin on maternal and fetal body composition we used magnetic resonance imaging and spectroscopy. This allowed us to quantify subcutaneous and intra-abdominal adipose tissue deposition and hepatic and skeletal muscle ectopic lipid deposition in the mother; and to measure subcutaneous adipose tissue deposition, hepatic lipid and hepatic volume in the fetus. To determine the effect of metformin on maternal endothelial function, we measured endothelium-dependent flow-mediated dilatation at the beginning and end of pregnancy. Change in diameter of the brachial artery in response to a flow stimulus created by arterial occlusion was measured using ultrasound imaging. We found no significant effect of metformin on birth weight. Mean birth weight was 3463 g (SD 660) in the placebo group and 3462 g (SD 548) in the metformin group (adjusted mean difference in z score –0·029, 95% CI –0·217 to 0·158; p=0·7597). Subjects taking metformin did demonstrate increased insulin sensitivity (M/I difference between means during high dose insulin of 0.02 [95% CI 0.001 to 0.03] milligrams per kilogram fat free mass per minute per pmol/L, p=0.04) but also enhanced endogenous glucose production (difference between means 0.54 [95% CI 0.08 to 1.00] milligrams per kilogram fat free mass per minute, p=0.02), compared with those taking placebo. We did not demonstrate any differences between treatment groups in maternal subcutaneous and intra-abdominal adipose tissue, or ectopic lipid deposition, or in fetal body fat distribution and liver volume. Participants in both treatment groups demonstrated a decline in endothelium-dependent flow-mediated dilatation between early and late pregnancy but there were no differences in the magnitude of that decline between the treatment groups. In conclusion, metformin, administered to obese, non-diabetic pregnant women, does not have any significant effect on birth weight of the baby. Our clamp studies demonstrated that subjects taking metformin were indeed more insulin-sensitive than those taking placebo, but the higher endogenous glucose production in this group suggests a reduced ability to suppress hepatic glucose production in response to insulin. This increased glucose flux may in part explain the lack of effect of metformin on fetal nutrition and growth. We can conclude that metformin, should not be used as an intervention in obese pregnant women to prevent excess birth weight. The global obesity epidemic is one of the greatest public health challenges we face and the cycle of disadvantage continues to be perpetuated to the next generation. The lack of any effective interventions for this high-risk group remains a significant concern and an important area for further research.

abstract: Background: Obesity is considered one of the most serious public health issues worldwide. Small, feasible lifestyle changes are necessary to obtain and maintain weight loss. Clinical evidence is inconclusive about whether meal preloading is an example of a small change that could potentially increase the likelihood of weight loss and weight maintenance. Objective: The aim of this study is to determine if consuming 23 grams of peanuts, as a meal preload, before a carbohydrate-rich meal will lower post prandial glycemia and insulinemia and increase satiety in the 2 hour period after a carbohydrate-rich meal. Design: 15 healthy, non-diabetic adults without any known peanut or tree nut allergies were recruited from a campus community. A randomized, 3x3 block crossover design was used. The day prior to testing participants refrained from vigorous activity and consumed a standard dinner meal followed by a 10 hour fast. Participants reported to the test site in the fasted state to complete one of three treatment meals: control (CON), peanut (NUT), or grain bar (BAR) followed one hour later by a carbohydrate-rich meal. Satiety, glucose and insulin were measured at different time points throughout the visit. Each participant had a one-week washout period between visits. Results: Glucose curves varied between treatments (p=.023). Blood glucose was significantly higher one hour after ingestion of the grain bar compared to the peanut and control treatments (p<.001). At 30 minutes after the meal, the control glucose was significantly higher than for the peanut or grain bar (p=.048). Insulin did vary significantly between treatments (p<.001). The insulin change one hour after grain bar consumption was significantly higher than after the peanut or control at the same time point (p<.001). The change in insulin one hour after peanut consumption was significantly higher than for the control treatment (p=.002). Overall satiety, expressed as the 180 minute AUC, differed significantly between treatments (p=.001). One hour after preload consumption, peanut and bar consumption was associated with greater satiety than the water control (p<.001). At 30 minutes post-meal, the grain bar was associated with greater satiety versus the water control (p=.049). The bar was also associated with greater satiety versus peanut and control at 60 and 90 minutes post-meal (p=.003 and .034, respectively). At 120 minutes post-meal, the final satiety measurement, the bar was still associated with greater satiety than the peanut preload (p=.023). Total energy intake, including test meal, on treatment days did not differ significantly between treatment (p=.233). Conclusions: Overall satiety, blood glucose and blood insulin levels differed at different time points depending on treatment. Both meal preloads increased overall satiety. However, grain bar ingestion resulted in sustained satiety, greater than the peanut preload. Grain bar ingestion resulted in an immediate glycemic and insulinemic response. However, the response was not sustained after the test meal was ingested. The results of this study suggest that a low-energy, carbohydrate-rich meal preload may have a positive impact on weight maintenance and weight loss by initiating a sustained increase in overall satiety. More research is needed to confirm these findings. / Dissertation/Thesis / M.S. Nutrition 2012

Women with raised BMIs ≥30kg/m2 have now become the ‘norm’ in maternity practice due to the recent obesity epidemic. To date only very limited research evidence exists highlighting midwives’ experiences of caring for this group of women. This thesis aims to provide original research on what it means to midwives and student midwives on the point of qualification to care for this client group throughout the childbirth continuum.

As the obesity epidemic continues to grow, attention has been turned towards the abundance of processed foods and beverages in the Western diet. Controversy has particularly surrounded high fructose corn syrup (HFCS), which is a commonly used sweetener in these products. Our study is designed to not only investigate the metabolic effects resulting from prolonged exposure to a highly sweetened diet, but also to determine the effects of this maternal diet on the offspring. For the study, three specially made, pelleted diets and a control were administered to weight matched groups of female Long Evans rats: Control "Chow" AIN-G93, Group (2) AIN-G93 + 10% HFCS, Group (3) AIN-G93 + 20% HFCS, and Group (4) 20% sucrose. All of the diets were isocaloric and differed only in the amount of added sweetener. At the end of the initial study, a strong phenotypic difference was not determined among the dams; however, postnatal body weights were increased in the pups born to dams raised on sweetened diets groups compared to the Chow-fed dams. Even further, following exposure to a LF or HF diet, the progeny showed altered sensitivity to the obesogenic effects of the diet as was seen in body weights and caloric intake. Glucose homeostasis, plasma triglyceride levels, and liver weights also appeared to be influenced by the maternal and post-weaning diets. To further examine this maternal diet effect, the study was repeated, and experiments were performed while the pups were in utero and also during lactation. Metabolic parameters measured during pregnancy showed a trend towards higher triglycerides in the HFCS dams compared to Chow. Tests during lactation aimed to determine whether the pups were hyperphagic, but showed no significance. Overall, these studies suggest that sweetener components such as sucrose or HFCS used in beverages and processed foods may potentially contribute to the development to the obesity and the metabolic syndrome in offspring. Additionally, HFCS may amplify this effect even further.