East Tennessee has one of the most rapidly growing Hispanic population in the country. Further, it has been previously reported that this population is at an increased risk for developing metabolic syndrome (MetS), which is characterized by central obesity, abnormal blood lipids, hypertension, insulin resistance, and glucose intolerance. Our collaborators at the Johnson City Community Health Center (JCCHC) observed these indicators of MetS even in young children, between the ages of two and ten. The principle objective of this research project was to examine the prevalence of risk factors for MetS and establish an expanded metabolic profile of young Hispanic children. These factors have not been previously examined in this population. Our working hypothesis is that even at a young age markers of MetS, specifically dysregulated hormone levels, are present in this pediatric population. Methods: In this cross-sectional analysis, a total of 118 Hispanic children between 2-10 years of age (Mean 6.4 ± 2.7, 45% male) age adjusted anthropometric measurements and blood samples were obtained. Blood samples were analyzed for glucose, and lipids (triglycerides, LDL (low density lipoprotein) and HDL (high density lipoprotein) cholesterol) and C-reactive protein through ETSU clinical labs. Insulin, adiponectin, leptin, ghrelin, CRP, IL-6, and TNF-a levels were measured using commercially available assays (Bio-Rad® Multiplex Immunoassay System). Results: There was a significant positive correlation with leptin and adiponectin levels and BMI. Further, children with 2 or more risk factors for metabolic syndrome (as determined by age- and sex-specific: waist circumference, blood pressure, HDL, and triglyceride measures) had significantly elevated leptin levels. The proportional relationship between these metabolic hormone levels and the central obesity indicator confirms that metabolic abnormalities are present in the pediatric Hispanic population at a young age in Northeast Tennessee. The predisposition for this demographic developing metabolic syndrome is evident with indicators being present so early in life. With Tennessee being ranked third in the nation for Hispanic population growth rate, these findings indicate a need for early age intervention protocols for Hispanic children in order to reduce their risk of developing metabolic syndrome.

Recently, the body mass of college football lineman has increased markedly and places them at higher risk for a number of postcompetitive pathogenic chronic health consequences. Recognition of problems associated with oversized athletes is easily accepted intellectually–however, the practicalities of solving the problem have not been fully realized.

Orientador: Marilza Vieira Cunha Rudge / Coorientador: Joelcio Francisco Abbade / Coorientador: Paulo Adão de Campos / Banca: Iracema de Matos Paranhos Calderon / Banca: Roberto Antonio de Araújo Costa / Banca: Carlos Antonio Negrato / Banca: Maria Leticia Sperandeo de Macedo / Não disponível / Not available / Doutor

Metabolic syndrome and its component conditions of hypertension, obesity, and insulin resistance are on the increase in United States. Metabolic syndrome substantially increases the risk of cardiovascular disease and type 2 diabetes (T2D). To date, no published study has examined the relationship between psychological traumas from physical and/or sexual assault in childhood and metabolic syndrome or its components. This study, using the psychoneuroimmunology (PNI) model, investigated associations between psychological trauma (physical/sexual abuse) in childhood and metabolic syndrome in adulthood using data from the Midlife in the United States II (MIDUS-II) study. This research was undertaken to investigate whether a history of psychological trauma was associated with an elevated risk for metabolic syndrome. Chi-square test and logistic regression were used to investigate the respective associations. Metabolic syndrome was the dependent variable, assault in childhood was the independent variable, and the relevant covariates included in the logistic regression model were age, gender, cigarette and alcohol consumption, and ethnicity. While there was no significant association between assault in childhood and metabolic syndrome (p = 0.146), there were significant associations between metabolic syndrome and age group (p =< 0.026). In the adjusted logistic regression model, the only covariate that showed significant association with metabolic syndrome was Age Group 2 (41-55; p = 0.016). Also significant was the association between sexual assault in childhood and high blood pressure (p = 0.041). The results of this study suggest that clinicians may wish to watch for evidence of abuse, given the potential for future health impacts.

Orientador: Camila Renata Corrêa / Banca: Janete Pessuto Simonetti / Banca: Dijon Henrique Salomé de Campos / Banca: Miriam Domingues Cardoso / Banca: Estela Maria Leite Meirelle Monteiro / Resumo: Introdução: A síndrome metabólica (SM) é uma doença atribuída à mudança do estilo de vida a qual tem atingido habitantes de diferentes locais. Objetivo: Investigar a prevalência de síndrome metabólica e fatores associados a ela nos moradores adultos do Arquipélago de Fernando de Noronha (PE-Brasil). Método: Foram avaliados em 363 indivíduos. Idade, medidas antropométricas, pressão arterial sistêmica, e exames bioquímicos foram avaliados. A SM foi diagnosticada de acordo com os critérios da International Diabetes Federation (IDF). Resultados: Dos 363 indivíduos 248 (68,3%) eram do sexo feminino e 115 (31,6 %) do sexo masculino, com a idade média de 43,3 ± 9,1 anos, peso médio de 75,3 ± 16,4kg. A prevalência de SM foi de 20,7%. Dentre os outros fatores associados a ela, a circunferência da cintura mostrou-se bastante elevada na população estudada, 253 indivíduos (69,7%). Quanto a pressão arterial sistêmica, 117 (32,2%) dos indivíduos eram hipertensos, glicemia de jejum alterada foi observada em 68 (18,7%) dos indivíduos, triglicérides em 70 (19,3%), HDLc em 76 (20,9%). A prática de atividade física apresentou-se baixa, apenas 103 (28,4%) praticavam algum tipo de exercício físico e 62 (17%) consumiam frutas e verduras, 47 (12,9%) eram tabagistas, 133 (36,6%) faziam o uso de bebidas alcoólicas e 207 (56,7%) consumiam água dessalinizada. Conclusão: A Síndrome Metabólica diagnosticada na população foi afetada pelo alto índice do aumento da circunferência da cintura, baixo consumo de frutas e verduras e pouca prática de atividade física. A população necessita de um programa abrangente e integrado de educação em saúde, com estímulos para inserir modos preventivos modificando seus hábitos de vida, incentivando o consumo de alimentos saudáveis, visando à conscientização da melhoria de qualidade de vida dos moradores da ilha / Abstract: Introduction: Metabolic syndrome (MS) is a disease attributed to lifestyle change which has affected people from different locations. Objective: To investigate the prevalence of metabolic syndrome and factors associated with it in the adult residents of the archipelago of Fernando de Noronha (PE-Brazil). Method: The study included 363 individuals. Age, anthropometric measures, blood pressure, and biochemical tests were evaluated. MS was diagnosed according to the criteria of the International Diabetes Federation (IDF). Results: Of 363 individuals 248 (68.3%) were female and 115 (31.6%) male, mean age 43.3 ± 9.1 years, mean weight of 75.3 ± 16,4kg. The prevalence of MS was (20.66%). Among the other factors associated with it, waist circumference proved to be very high in the study population, 253 individuals (69.69%). As for blood pressure, 117 (32.23%) individuals were hypertensive, impaired fasting glucose was observed in 68 (18.73%) of subjects, triglycerides by 70 (19.28%), HDL-C 76 (20.93%). The low physical activity presented itself, only 103 (28.37%) practice some form of physical exercise and 62 (17%) consume fruits and vegetables, 47 (12.94%) were smokers, 133 (36.63%) were using alcohol and 207 (56.74%) consumed desalinated water. Conclusion: Metabolic syndrome diagnosed in the population was affected by the high rate of increase in waist circumference, low consumption of fruits and vegetables, little physical activity. The population needs a comprehensive and integrated program of health education, with incentives to enter preventive modes modifying your lifestyle habits by encouraging the consumption of healthy foods, aimed at raising awareness of improved quality of life for residents of the island / Doutor

A reprogramação fenotípica causada por alterações ambientais distintas associada ao alto consumo de frutose na idade adulta poderia contribuir para o agravamento de distúrbios metabólicos. Para avaliar se a exposição pré-natal à dexametasona (DEX) modula os efeitos do consumo de frutose sobre o metabolismo hepático, investigamos a prole masculina nascida de ratas Wistar tratadas ou não com DEX (0,2mg/kg massa corpórea/dia) no 3°período gestacional. As proles de mãe controle (sem tratamento) e mães tratadas com DEX foram mantidas sem frutose (CTL e DEX) ou foram suplementadas com solução de frutose a 10% durante 8 semanas (frutose e DEX+frutose). Tanto os grupos frutose quanto DEX+frutose apresentaram consumo de frutose semelhante, intolerância à glicose e aumento da atividade máxima da enzima glicolítica PFK. Apenas DEX+frutose apresentou aumento dos triglicérides hepáticos e acúmulo de lipídeos intra-hepáticos. Além disso, o grupo DEX+frutose não mostrou expressão aumentada dos genes sec22, mttp e apoB, envolvidos na síntese, montagem e secreção de VLDL; paralelamente, observamos diminuição na concentração de triglicérides em 6 horas após injeção de Tyloxapol comparado ao DEX e frutose. Ainda, apresentou diminuição da expressão de BECLIN1, da expressão gênica de HSP90, e alteração de marcadores moleculares relacionados ao HCC, como diminuição de TP53, P21 e TIGAR, e aumento da expressão de mRNA afp e hsp70. Em conjunto, nossos dados indicam que a exposição à DEX in útero leva a uma resposta metabólica única frente a alta ingestão de frutose na vida adulta. O aumento da gliconeogênese e intolerância à glicose, a redução na produção e secreção de VLDL e o prejuízo no fluxo autofágico estimulam o acúmulo de gotículas lipídicas no fígado que pode favorecer o desenvolvimento de HCC em resposta à alta ingestão de frutose. / Phenotypic programming caused by distinct environmental changes and associated with high fructose consumption in adulthood could contribute to the worsening of metabolic disorders. To evaluate whether prenatal exposure to Dexamethasone (DEX) modulates the effects of fructose consumption on hepatic metabolism, we investigated male offspring born to Wistar rats treated with or without DEX (0.2 mg / kg body weight / day) at 3rd gestational period. The offspring of control (untreated) and DEX treated mothers were maintained without fructose (CTL and DEX) or supplemented with 10% fructose solution for 8 weeks (fructose and DEX+fructose). Both the fructose and DEX+fructose groups showed similar fructose consumption, glucose intolerance and increased maximal activity of the glycolytic enzyme PFK. Only DEX+fructose presented increase in hepatic triglycerides and accumulation of intrahepatic lipids. In addition, the DEX + fructose group did not show increased expression of sec22, mttp and apoB genes involved in the synthesis, assembly and secretion of VLDL; in parallel, we observed a decrease in TG concentration in 6 hours after injection of Tyloxapol, compared to DEX and fructose. In addition, there was a decrease in BECLIN1 expression, HSP90 gene expression, and alteration of HCC-related molecular markers such as TP53, P21 and TIGAR, and increased expression of afp and hsp70 mRNA. Taken together, our data indicate that exposure to DEX in utero leads to a unique metabolic response to high fructose intake in adult life. Increased gluconeogenesis and glucose intolerance, reduction in VLDL production and secretion, and loss of autophagic flow stimulate the accumulation of lipid droplets in the liver, that may favor the development of HCC in response to high fructose intake.

The insulin resistance syndrome [INSR] is associated with increased cardiovascular risk and affects up to 25% of the Australian population. The mechanism underlying the relationship between the INSR and increased cardiovascular risk is controversial. We postulated that perturbations in the renin-angiotensin system [RAS] and endothelium-derived NO may be implicated in the development of early vascular changes in the INSR. Repeated measurements of arterial stiffness [using digital photoplethysmography] and haemodynamic parameters in response to vasoactive medications were used to demonstrate the functional expression of angiotensin II [Ang II] receptors and NO synthase [NOS]. Ang II acts via two main receptor sub-types: the Ang II type 1 [AT1] and Ang II type 2 [AT2] receptors. The AT1 receptor is central to the development of arterial stiffness and endothelial dysfunction. The role of AT2 receptors in humans is controversial but is postulated to counter-act AT1 receptor mediated effects in diseased vascular beds. We demonstrated increased AT1 and AT2 receptor-mediated effects in small to medium-sized arteries of subjects with early INSR [Chapter 6]. In addition, functional expression of AT2 receptors in adult insulin resistant humans [Chapter 5], but not in healthy volunteers [Chapter 4] was demonstrated. AT1 receptor blockade in subjects with early INSR resulted in improvements in vascular function, with a consequent functional down-regulation of AT2 receptors [Chapter 7]. Functional NOS expression was demonstrated to be increased in subjects with early INSR compared with healthy controls [Chapter 6]. This was postulated to be a homeostatic response to counteract early vascular changes in subjects with early INSR. AT1 receptor blockade in these subjects reduced functional NOS expression [Chapter 8]. In conclusion, patients with early INSR represent a model of early disease where early intervention may be able to reverse the process incited by the initial exposure to multiple cardiovascular risk factors. Early vascular changes in these individuals are mediated at least in part, by increased AT1 receptor activity and/or expression, and may be detected by changes in arterial stiffness indices and non-invasive vascular reactivity studies. There is a compensatory increase in AT2 receptor and NOS expression/activity to counter-act these vascular changes.

The insulin resistance syndrome [INSR] is associated with increased cardiovascular risk and affects up to 25% of the Australian population. The mechanism underlying the relationship between the INSR and increased cardiovascular risk is controversial. We postulated that perturbations in the renin-angiotensin system [RAS] and endothelium-derived NO may be implicated in the development of early vascular changes in the INSR. Repeated measurements of arterial stiffness [using digital photoplethysmography] and haemodynamic parameters in response to vasoactive medications were used to demonstrate the functional expression of angiotensin II [Ang II] receptors and NO synthase [NOS]. Ang II acts via two main receptor sub-types: the Ang II type 1 [AT1] and Ang II type 2 [AT2] receptors. The AT1 receptor is central to the development of arterial stiffness and endothelial dysfunction. The role of AT2 receptors in humans is controversial but is postulated to counter-act AT1 receptor mediated effects in diseased vascular beds. We demonstrated increased AT1 and AT2 receptor-mediated effects in small to medium-sized arteries of subjects with early INSR [Chapter 6]. In addition, functional expression of AT2 receptors in adult insulin resistant humans [Chapter 5], but not in healthy volunteers [Chapter 4] was demonstrated. AT1 receptor blockade in subjects with early INSR resulted in improvements in vascular function, with a consequent functional down-regulation of AT2 receptors [Chapter 7]. Functional NOS expression was demonstrated to be increased in subjects with early INSR compared with healthy controls [Chapter 6]. This was postulated to be a homeostatic response to counteract early vascular changes in subjects with early INSR. AT1 receptor blockade in these subjects reduced functional NOS expression [Chapter 8]. In conclusion, patients with early INSR represent a model of early disease where early intervention may be able to reverse the process incited by the initial exposure to multiple cardiovascular risk factors. Early vascular changes in these individuals are mediated at least in part, by increased AT1 receptor activity and/or expression, and may be detected by changes in arterial stiffness indices and non-invasive vascular reactivity studies. There is a compensatory increase in AT2 receptor and NOS expression/activity to counter-act these vascular changes.

The insulin resistance syndrome [INSR] is associated with increased cardiovascular risk and affects up to 25% of the Australian population. The mechanism underlying the relationship between the INSR and increased cardiovascular risk is controversial. We postulated that perturbations in the renin-angiotensin system [RAS] and endothelium-derived NO may be implicated in the development of early vascular changes in the INSR. Repeated measurements of arterial stiffness [using digital photoplethysmography] and haemodynamic parameters in response to vasoactive medications were used to demonstrate the functional expression of angiotensin II [Ang II] receptors and NO synthase [NOS]. Ang II acts via two main receptor sub-types: the Ang II type 1 [AT1] and Ang II type 2 [AT2] receptors. The AT1 receptor is central to the development of arterial stiffness and endothelial dysfunction. The role of AT2 receptors in humans is controversial but is postulated to counter-act AT1 receptor mediated effects in diseased vascular beds. We demonstrated increased AT1 and AT2 receptor-mediated effects in small to medium-sized arteries of subjects with early INSR [Chapter 6]. In addition, functional expression of AT2 receptors in adult insulin resistant humans [Chapter 5], but not in healthy volunteers [Chapter 4] was demonstrated. AT1 receptor blockade in subjects with early INSR resulted in improvements in vascular function, with a consequent functional down-regulation of AT2 receptors [Chapter 7]. Functional NOS expression was demonstrated to be increased in subjects with early INSR compared with healthy controls [Chapter 6]. This was postulated to be a homeostatic response to counteract early vascular changes in subjects with early INSR. AT1 receptor blockade in these subjects reduced functional NOS expression [Chapter 8]. In conclusion, patients with early INSR represent a model of early disease where early intervention may be able to reverse the process incited by the initial exposure to multiple cardiovascular risk factors. Early vascular changes in these individuals are mediated at least in part, by increased AT1 receptor activity and/or expression, and may be detected by changes in arterial stiffness indices and non-invasive vascular reactivity studies. There is a compensatory increase in AT2 receptor and NOS expression/activity to counter-act these vascular changes.

<p>A quart of the of the adult population worldwide have</p><p>metabolic syndrome. A sedentary lifestyle, low physical</p><p>activity, combined with wrong eating habits, stress,</p><p>smoking and psychosocial factors, are the main causes of</p><p>development of the metabolic syndrome. The purpose of</p><p>the literature review was to illuminate the physical</p><p>activity in persons who have the metabolic syndrome, and</p><p>what sort of advice a nurse use in the promotion of</p><p>physical activity. The study was conducted as a literature</p><p>review, including 15 scientific quantitative articles. In ten</p><p>articles, the focus was on physical activity at the</p><p>metabolic syndrome, and five articles focused on various</p><p>forms of counselling for physical activity. The results</p><p>showed that there is a strong correlation between level of</p><p>physical activity and risk of developing metabolic</p><p>syndrome. Increased physical activity reduces the risk of</p><p>developing metabolic syndrome and has positive effects</p><p>on metabolic risk factors. Physical activity may be crucial</p><p>for the prevention of metabolic syndrome. Advice via</p><p>telephone, e-mail and physical activity on prescription is</p><p>effective method for the promotion of physical activity.</p><p>This study also showed that the nurse has an important</p><p>role in promoting physical activity. Promotion of physical</p><p>activity should be given a clearer place in health care.</p>