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

Thesis (Ph. D.)--University of Texas at Austin, 2004. / Supervisor: Jeanne H. Freeland-Graves. Vita. Includes bibliographical references.

Master of Science / Department of Agricultural Economics / Vincent Amanor-Boadu / Metabolic syndrome (MetS) continues to be a public health concern in the United States. The current prevalence rate is about 34% among American adults. One of the recommended line of treatment for the components of MetS is dietary behavior change. Although, many dietary recommendations guidelines are published to aid in better dietary choices, little is known about how effectively they alter dietary choices. Thus, the overall objective of this study was to examine the extent to which knowledge about the presence of metabolic syndrome components influenced macronutrient intake. Data from 2013-2014 National Health and Nutrition Examination Survey (NHANES) were used for the study. The variables used were taken from modules of the NHANES dataset: demographic, dietary (day 1 and 2 recall), questionnaire (blood Pressure & Cholesterol, medical condition, diabetes and weight history), examination (blood pressure and body measures) and laboratory (cholesterol – high density lipoprotein, and triglycerides and plasma fasting glucose). Daily macronutrients (calories, protein, carbohydrate, fat and total sugar) intake were regressed on knowledge of MetS components presence and demographic characteristics using Ordinary Least Square model. The results show that having information that one has diabetes was associated with a reduced intake of daily calories (160 kcal), carbohydrate (22.73 g) and total sugar (15.26 g). There was no significant association between protein and fat intakes and the knowledge of the presence of a metabolic syndrome component in the econometric model. Ageing was associated with increase in calorie (16 kcal/day), protein (0.502 g/day) and fat (0.66 g/day) intake. Males consumed higher amounts of all macronutrients than females. Higher education was associated with higher fat intake (5.09 g/day for High School and 4.54 g/day for college compared with those with less than high school education) but reduced sugar intake (8.86 g/day) for those with college education. It was found that 27.59% of individual’s who had diabetes did not know they had it, and about 41% of those who did know they were overweight had central obesity. The study concludes that compared to knowledge about high triglyceride levels, low high-density lipoprotein, diabetes, high blood pressure and overweight, knowledge about having diabetes seems to motivate people to change their dietary intake. This may be due to the immediate effect of diet on diabetic patients compared to the other MetS components. The result of this is that it may be appropriate to pursue drug therapy for addressing the other MetS components while diet change may be effective contributor to managing diabetes.

Non-alcoholic fatty liver disease (NAFLD) is the most common cause of liver dysfunction in the western world and one of the main contributors to cirrhosis and potentially liver cancer and liver failure. A variety of behaviors and other factors can predispose certain individuals to an increased risk of developing NAFLD and non-alcoholic steatohepatitis (NASH). These factors include, but are not limited to, obesity, insulin resistance, hyperglycemia, and high levels of fat in the blood. The result is the accumulation of fat in hepatocytes that over time leads to inflammation and scarring of the liver and ultimately liver damage. At present, the mainstay of therapy remains weight loss through dietary modification and lifestyle change. Due to the lack of specific targeted pharmacotherapies, there is great interest from the scientific community to find a potential therapy that can provide benefit to the many patients in need. Some existing medications, including pioliglitazones and angiotensin receptor antagonists, may be repurposed to help treat this condition. Vitamin E may improve the histology in NASH, but safety issues limit its use. Other drugs, such as farnesoid X receptor agonist, obeticholic acid, are also in clinical trials with great hope for the future. However, as the cause of NAFLD and thereby NASH is poorly understood, there is a need for further research in the field to better understand the pathophysiology of the disease and the potential for pharmacotherapy for treatment of the disease. There has, however, been evidence that the antidiabetic drug class known as glucagon-like receptor agonists (GLP-1 RAs) has been shown to reduce liver damage in patients with non-alcoholic steatohepatitis. Liraglutide, currently a drug for type 2 diabetes and obesity, has been shown to provide great benefit in type 2 diabetes and obesity and after reviewing multiple studies, seems to provide a potential treatment also for patients with NAFLD and NASH. However, more research needs to be done to confirm this hypothesis. Its more potent version, called semaglutide, is currently in phase 2 clinical trials and provides great hope in potentially further reducing liver damage. This class of drugs provides a huge opportunity to address an unmet clinical need that could benefit millions of patients worldwide. .

Chronic glucocorticoid (GC) excess (Cushing’s syndrome, pharmacotherapy) causes metabolic and cardiovascular disease. This might be predicted from the known metabolic (dyslipidaemia, insulin resistance/hyperglycaemia) and hypertensive effects of chronically elevated GC levels. Intracellular GC levels within target tissues are controlled by 11β-hydroxysteroid dehydrogenases. 11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1, encoded by Hsd11b1) is an enzyme that, in intact cells and in vivo, converts inert GCs (cortisone in humans, and 11- dehydrocorticosterone in mice and rats) into their active forms (cortisol and corticosterone, respectively). Consequently, 11β-HSD1 amplifies intracellular GC levels. Additionally, 11β-HSD1 is also involved in the metabolism of 7-oxysterols; it catalyses the reduction of 7-ketocholesterol (7-KC) to 7β-hydroxycholesterol (7β- HC). 7-KC may inhibit cholesterol biosynthesis through its ability to inhibit cleavage/processing of sterol regulatory element binding protein-2 (SREBP-2), the key regulator of cholesterol synthesis. Alteration of cholesterol homeostasis is a major risk factor for cardiovascular disease. Improvement of metabolic syndrome and attenuation of atherosclerosis are observed in susceptible rodent models with 11β- HSD1 deficiency or inhibition. Conversely, pilot data showed decreased levels of 7- KC as well as increased levels of cleaved SREBP-2 protein (the transcriptionally active form) in liver of mice with hepatic 11β-HSD1 overexpression (LOE mice), suggesting increased cholesterol biosynthesis. It was hypothesised that hepatic 11β- HSD1 promotes cholesterol biosynthesis through hepatic induction of SREBP-2 target genes in the cholesterol biosynthetic pathway. The hypothesis was tested in adult, male LOE and wild-type C57BL/6 mice. In mice fed a standard chow diet, hepatic levels of mRNA encoding hydroxymethylglutarylcoenzyme A (HMG-CoA) reductase and HMG-CoA synthase, SREBP-2 targets in the cholesterol biosynthetic pathway, did not differ between genotypes. Compared to chow, a cholesterol-rich ‘Western’ diet (WD) decreased hepatic levels of mRNA encoding SREBP-2, HMG-CoA reductase and HMG-CoA synthase in wild-type as well as in LOE mice. These data imply that LOE mice show a normal physiological response with respect to cholesterol synthesis when challenged with cholesterol-rich diet, and, contrary to the hypothesis, liver 11β-HSD1 does not increase cholesterol biosynthesis via elevated expression of mRNAs encoding hepatic cholesterol biosynthetic enzymes. The liver X receptors (LXR) are well-known as sensors of oxysterols and regulators of genes involved in processes that decrease total body cholesterol levels i.e. reverse cholesterol transport and cholesterol excretion into bile. Cholesterol is the precursor to oxysterol LXR ligands. It was predicted that liver overexpression of 11β-HSD1 leads to activation of LXRα (the isoform with dominant roles in reverse cholesterol transport and whole-body cholesterol homeostasis) and its downstream targets involved in cholesterol efflux and excretion, in response to increased intracellular cholesterol levels. Indeed, levels of Lxrα mRNA were increased in livers of WD-fed LOE mice compared to wild-type mice on the same diet. There was no evidence for increased cholesterol clearance through bile acid synthesis in LOE mice as indicated by unchanged levels of hepatic Cyp7a1 mRNA between LOE and wild-type mice. However, consistent with being direct targets of LXRα, increased Abcg5 and Abcg8 mRNA levels were observed in livers of WD-fed LOE mice compared to WD-fed wild-type mice. These results corroborate findings in chow-fed LOE mice. Moreover, these data suggest that LOE mice ‘sense’ intracellular cholesterol excess and respond to it by increasing cholesterol efflux into the biliary lumen for excretion, thereby supporting a role for hepatic 11β-HSD1 in promoting biliary cholesterol secretion. To assess the effect(s) of hepatic 11β-HSD1 deficiency on cholesterol homeostasis as well as evaluate the importance of liver 11β-HSD1 in metabolic syndrome, liver-specific 11β-HSD1 knockout (LKO) mice were generated by crossing “floxed” Hsd11b1 mice with Alb-Cre transgenic mice in which Cre expression is restricted to hepatocytes. In liver of LKO mice, 11β-HSD1 mRNA, protein and enzyme activity were reduced by >80%, with no differences in 11β-HSD1 protein levels in kidney, adipose tissue or muscle between LKO and floxed Hsd11b1 littermate controls. These results indicate liver-specificity of Hsd11b1 knockdown in these mice. Body weight and weights of liver, adipose tissue, adrenal, muscle, kidney and brain were unaltered by liver-specific 11β-HSD1 deficiency on a standard chow diet. These mice were subject to a 14-week high fat (HF) diet, which typically causes metabolic syndrome in control but not globally 11β-HSD1 deficient mice. In HF-fed LKO mice, weights of the subcutaneous and epididymal fat depots were decreased compared to HF-fed control mice, resulting in an overall decrease in total white adipose tissue weight. Although no differences were observed in subcutaneous adipocyte hypertrophy between HF-fed LKO and control mice in a small number of samples tested, the above finding suggests that liver 11β-HSD1 influences adiposity and that liver-specific deficiency of 11β-HSD1 may reduce diet-induced adiposity. In terms of cholesterol homeostasis, no differences were observed in hepatic levels of mRNAs encoding cholesterol biosynthetic enzymes as well as those encoding enzymes/transporters for cholesterol catabolism/excretion between LKO and control mice, on either chow or HF diet. In summary, these data do not support a role for hepatic 11β-HSD1 in cholesterol synthesis. However, my evidence suggests that increased hepatic 11β-HSD1 promotes hepatobiliary cholesterol secretion. Finally, knockdown of liver 11β-HSD1, combined with HF feeding, reduces adiposity, suggesting that hepatic 11β-HSD1 may play a key role in adipose tissue lipogenesis/lipolysis and/or lipid storage, and that liver-specific 11β-HSD1 inhibition (or deficiency) may be advantageous in diet-induced obesity. Data presented in this thesis contribute to the understanding of the role of hepatic 11β-HSD1 in cholesterol homeostasis and metabolic syndrome.

Obesity, metabolic syndrome, and diabetes represent a major source of morbidity and mortality in the United States and worldwide. Chronic misalignment of an organism’s internal circadian clock with diurnal, cyclic changes in the external environment, prevalent in professions that require shift work, contributes significantly to Type 2 Diabetes development. Experimentally, only short-term models of circadian disruption have been explored. Therefore, the goal of this study was to establish an animal model of chronic circadian disruption, which would more closely mimic the harmful misalignment associated with metabolic syndrome in clinical studies. Moreover, since high fat diet consumption alters circadian behavior and rhythmic gene expression, contributing to the diet-induced phenotype, I hypothesized that chronic circadian disruption interacts with a high fat diet to worsen metabolic syndrome. To investigate circadian misalignment and diet-induced metabolic syndrome, I examined the contribution of the Aryl Hydrocarbon Receptor (AhR). AhR has similar PAS domain containing motifs as circadian clock proteins allowing for protein/protein interactions and crosstalk between AhR signaling and circadian rhythms. Furthermore, AhR activation is implicated in Type 2 Diabetes risk. To examine chronic circadian disruption, male wild-type (WT; C57Bl/6J) and AhR +/- mice were entrained to 12/12-hour light/dark cycles where lights were on from 10pm-10am and off from 10am-10pm. Misalignment was initiated by delaying the time of lights on by 8 hours on Monday. Mice were exposed to the misalignment schedule Monday-Friday then returned to the entrainment schedule Saturday and Sunday to mimic readjustment to society during the weekend. Circadian misaligned mice were exposed to the altered light schedule for 15 weeks and control animals remained on the12/12-hour light/dark cycle. Mice were fed a normal chow diet (10% fat) or a high fat diet (60% fat). Animals were sacrificed and samples were collected at 4-hour intervals on day 2 of the weekend. Exposure to chronic circadian misalignment by light disruption or high fat diet altered circadian rhythms of behavior, metabolic outputs, and expression of circadian clock, clock-controlled nuclear receptor, and lipid metabolism genes. A combination of light misalignment and high fat diet exacerbated the effects of either treatment alone further disrupting behavior, enhancing % body fat and fasting glucose, and dampening circadian clock gene expression. AhR +/- mice also were protected from the metabolic consequences of chronic misalignment and a high fat diet by resistance to altered behavioral and molecular circadian rhythms and disruption of metabolic outputs. With metabolic syndrome and Type 2 Diabetes occurrence on the rise, it is important to understand all contributing factors, including circadian disruption. Differences between chronic circadian misalignment and high fat diet-induced obesity in WT and AhR +/- mice furthers our understanding of the complex mechanisms that underlie Type 2 Diabetes development and advocates the discovery of potential therapeutic targets for the development of novel treatment options.

Made available in DSpace on 2014-06-11T19:29:33Z (GMT). No. of bitstreams: 0 Previous issue date: 2011-02-24Bitstream added on 2014-06-13T18:39:14Z : No. of bitstreams: 1 nicola_m_me_botfm.pdf: 407001 bytes, checksum: d2df4d7f944f99c1f3db242c773a0c60 (MD5) / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / A prevalência crescente de hipertensão arterial é perpetuada por fatores comportamentais tais como dieta inadequada e inatividade física. Determinar os fatores associados à hipertensão arterial em adultos clinicamente triados para programa de mudança de estilo de vida. Foram estudados 1041 indivíduos, de ambos os sexos, com idade entre 26 a 88 anos, voluntários de programa de mudança de estilo de vida. A avaliação da pressão arterial foi realizada obedecendo a VI Diretriz Brasileira de Hipertensão Arterial. Colesterol total e frações, triglicerídios, glicemia, uréia, creatinina, ácido úrico e albumina foram analisados pelo método de Química Seca e proteína C reativa por imunoquimioluminescência. A avaliação antropométrica foi composta pelas medidas de circunferência abdominal, massa e estatura, com posterior cálculo do índice de massa corporal, e o percentual de gordura foi obtido por bioimpedância. A ingestão dietética foi realizada pelo recordatório de 24 horas, com posterior cálculo das porções da pirâmide e Índice de Alimentação Saudável adaptado. A avaliação cardiorrespiratória em esteira ergométrica foi feita pelo teste de Balke modificado. Análises estatísticas foram realizadas utilizando o programa SAS versão 9.2 e descritos em média e desvio padrão. Foi realizado o teste de Wilcoxon com normalidade da amostra sendo avaliada pelo teste de Shapiro-Wilk, e regressão linear com intervalo de confiança de 95%. Os resultados foram discutidos com base no nível de significância de p<0,05. O total de hipertensos atingiu 37,7% sendo 20,8% em uso de hipotensores medicamentosos. Não houve influência significativa da renda e da ingestão dietética sobre a prevalência de hipertensão. Por outro lado houve associação da obesidade e da adiposidade (corporal e abdominal) assim como da hiperglicemia e hipercolesterolemia. Na ausência... / The growing prevalence of hypertension is mainly due to happens by behavioral factors, such as inappropriate diet and physical inactivity. These study aims to determine the associated factors of hypertension in clinically screened adults a lifestyle modification program. One thousand and forty one volunteers were studied, both male and female, between 26 and 88 years old. The blood pressure was measured following VI Hypertension Brazilian Guideline. Plasma total cholesterol, triglycerides, glucose, urea, creatinine, uric acid and albumin were analyzed by the dry chemistry method and C-reactive protein by immunechemmiluminescence. The anthropometric evaluation consisted of weight and height measurements, with subsequent body mass index calculation. Fat percentage was obtained by electrical bioimpedance. Dietary intake was evaluated by a 24-hour food recall, with posterior pyramid servings and the adapted health eating index calculation. The cardiorespiratory fitness evaluation on treadmill was done by the modified Balke test. Statistic analyses were done using the 9.2 version SAS program and described in mean and standard deviation. The Wilcoxon test was done with normality sample being evaluated by the Shapiro-Silk test and linear regression with 95% confidence intervals. The results were discussed based on the significance level of p<0.05. The total number of hypertensive individuals was 37.7%, 20% of them taking anti-hypertensive medicine. There wasn’t significant influence of income and dietary intake concerning hypertension prevalence. On the other hand, there was an association of obesity and adiposity (corporal and abdominal) as well as of hyperglycemia and hypercholesterolemia. In the absence of medicine the hypertensive individuals showed similar age and body mass index values, higher of abdominal circumference (female) and glucose and lower of VO2max (female)... (Complete abstract click electronic access below)

Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgico / A associaÃÃo entre disfunÃÃes tireoideanas clinicamente manifestas e o desenvolvimento de distÃrbios metabÃlicos està bem determinada. Entretanto, nos Ãltimos anos, o debate acerca da relaÃÃo entre alteraÃÃes na funÃÃo tireoideana (FT) e a sÃndrome metabÃlica (SM), ou seus componentes, tem ganhado especial atenÃÃo. Sendo o hormÃnio tireoestimulante (TSH) o teste de rastreamento mais sensÃvel para a detecÃÃo de alteraÃÃes da FT, tem se discutido critÃrios mais rigorosos de normalidade em indivÃduos sadios, a partir do achado de associaÃÃo de desfechos clÃnicos desfavorÃveis com valores anteriormente considerados normais. No entanto, torna-se difÃcil a definiÃÃo de âsaÃdeâ, em especial no Ãmbito relacionado à adiposidade corporal, considerando ser a obesidade uma condiÃÃo de elevada prevalÃncia e per si relacionada a inÃmeras morbidades. Assim, este trabalho objetivou avaliar a relaÃÃo entre os elementos definidores da SM e a FT e determinar o valor de referÃncia (VR) do TSH em uma amostra de indivÃduos saudÃveis, do ponto de vista tireoideano, residentes na cidade de Fortaleza-CE, Brasil. Trata-se de um estudo transversal conduzido no perÃodo de marÃo de 2009 a janeiro de 2010 onde foram incluÃdos 267 indivÃduos eutireoideanos, selecionados a partir de critÃrios clÃnicos e laboratoriais. Esta seleÃÃo compreendeu quatro etapas incluindo o preenchimento de um questionÃrio auto-administrado, avaliaÃÃo mÃdica e laboratorial, com antropometria, medida da circunferÃncia abdominal (CA), da pressÃo arterial sistÃlica (PAS) e diastÃlica (PAD), determinaÃÃo sÃrica de TSH, tiroxina livre (T4l), triiodotironina (T3), anticorpo anti-tireoperoxidase (ATPO), anticorpo anti-tireoglobulina (ATG), glicose em jejum (GJ), insulina, colesterol total (CT), LDL, HDL e triglicerÃdeos (TG), cÃlculo da resistÃncia à insulina, atravÃs do modelo de avaliaÃÃo da homeostase (HOMA-IR), e a realizaÃÃo de ultrassonografia tireoideana (UST). Dentre os 267, foram selecionados 125 participantes, denominados indivÃduos-referÃncia, caracterizados por T4l e T3 normais, anticorpos anti-tireoideanos negativos e UST normal. Este grupo compÃs o banco de registros individuais necessÃrios para a determinaÃÃo do VR do TSH de acordo com as recomendaÃÃes do NCCLS e NACB guidelines. Os dados foram submetidos à anÃlise estatÃstica, atravÃs do software Statistical Package for the Social Sciences (SPSS), versÃo 14.0 para Windows&#61666;, sendo usados o teste t de Student, teste de Mann-Whitney para comparaÃÃo das variÃveis contÃnuas, o teste do qui-quadrado para variÃveis categÃricas e o teste de Spearman para anÃlise de correlaÃÃes, sendo adotado o nÃvel de significÃncia estatÃstica de 5% (p<0,05). Modelos de regressÃo linear mÃltipla foram aplicados na avaliaÃÃo das associaÃÃes entre a FT com as concentraÃÃes de lipÃdeos sÃricos e com vÃrios traÃos da SM, com e sem ajuste para idade, sexo e HOMA-IR. Para determinaÃÃo do intervalo de referÃncia do TSH foram adotados os percentis 2,5% e 97,5% da curva de distribuiÃÃo deste analito, como sendo os correspondentes dos limites inferior e superior do VR do TSH. ApÃs a anÃlise, observou-se que 77,2% dos indivÃduos eutireoideanos apresentaram pelo menos um elemento definidor da SM. Quanto Ãs relaÃÃes entre os parÃmetros metabÃlicos e a FT, observou-se correlaÃÃo positiva do TSH apenas com CA e PAD, enquanto o T4l correlacionou-se inversamente com quatro (CA, GJ, TG, PAD) dos cinco elementos definidores da SM. Ainda foi demonstrada uma clara correlaÃÃo inversa entre o status de FT e o HOMA-IR. A partir destes achados, especula-se que de fato exista uma associaÃÃo entre a FT e a SM, e que os nÃveis sÃricos de hormÃnios tireoideanos (HTs), mais do que TSH, estÃo relacionados com fatores de risco cardiovascular. Na determinaÃÃo do intervalo de referÃncia do TSH, os valores obtidos se encontram entre 0,56 a 4,45mUI/l, o que està em consonÃncia com os pontos previamente estabelecidos em estudos de base populacional. / The association between clinically overt thyroid dysfunction and the development of metabolic disorders is well established. However, in recent years, the debate about the relationship between changes in thyroid function (TF), the metabolic syndrome (MS) or its components has gained special attention. Since the thyroid stimulating hormone (TSH) screening test more sensitive for detecting changes in TF, has been discussed more stringent criteria of normality in healthy individuals, from the finding of an association of adverse clinical outcomes with values previously considered normal. However, it is difficult to define "health", particularly in relation to body adiposity, whereas obesity is a condition of high prevalence itself linked to numerous illnesses. This study aimed to evaluate the relationship between the defining elements of MS and changes in the TF and determine the reference value (RV) of TSH in a sample of healthy subjects, from the stand point of thyroid, in the city of Fortaleza, Brazil. This is a cross-sectional study conducted from March 2009 to January 2010 which included 267 euthyroid subjects were selected from clinical and laboratory criteria. This team comprised four stages including the completion of a self-administered questionnaire, laboratorial and medical evaluation, with anthropometry, measurement of waist circumference (WC), systolic blood pressure (SBP) and diastolic (DBP), determination of serum TSH, free thyroxine ( FT4), triiodothyronine (T3), anti-thyroperoxidase (ATPO), thyroglobulin antibody (ATG), fasting glucose (FG), insulin, total cholesterol (TC), LDL, HDL and triglycerides (TG), insulin resistance calculated by homeostasis model assessment (HOMA-IR ), and the realization of thyroid ultrasound (TUS). Among the 267, 125 participants were selected, named individuals-reference, characterized by normal FT4, anti-thyroid antibody negative and normal TUS normal. This group composed the database of individual records necessary for determining the VR TSH according to the NCCLS and NACB guidelines. Data were subjected to statistical analysis (software Statistical Package for the Social Sciences (SPSS), versÃo 14.0 para Windows&#61666;) being used the Student t test, Mann-Whitney test to compare continuous variables, the chi-square test for categorical variables and Spearman test for correlation analysis, adopting the statistical significance level of 5% (p < 0.05). Multiple linear regression models were applied to evaluate the associations between the FT with the concentrations of serum lipids and various traits of MS, with and without adjustment for age, sex, and HOMA-IR. To determine the reference range of TSH were adopted percentiles 2.5% and 97.5% of the distribution curve of the analyte, as the correspondents of the lower and upper limits of TSH RV. After the analysis, we observed that 77.2% of euthyroid subjects had at least one defining element of MS. Regarding the relationships between metabolic parameters and FT, there was positive correlation of TSH with only WC and DBP, while the FT4 correlated inversely with four (WC, FG, TG, DBP) in the five defining elements of MS. Yet been demonstrated a clear inverse correlation between the status of TF and HOMA-IR. From these findings, we speculate that in fact there is an association between the TF and MS, and that serum levels of thyroid hormones (THs) more than TSH, are related to cardiovascular risk factors. In determining the reference range of TSH, the values are between 0.56 to 4.45 mIU / l, which is in line with the points previously established in population-based studies.

Class of 2014 Abstract / Specific Aims: To determine the prevalence of metabolic syndrome (MetS) in patients treated in an outpatient clinic that were taking atypical antipsychotics. Methods: This retrospective chart review included 822 adults diagnosed with various personality/mood disorders. Age, gender, ethnicity, blood pressure, height, weight, lipid panels, fasting blood glucose, and second-generation antipsychotic (SGA) used and treatment length were obtained. Patients were separated into two groups: those who were not taking an SGA in/for the past three months (group 1), and those taking at least one SGA for a minimum of three months (group 2). MetS was determined using NCEP ATP III guidelines. The primary outcome measured was the difference in the prevalence of MetS between each group. Main Results: At baseline, 753 patients were in group 1 and 69 patients were in group 2, there was a higher percentage of females in group 1 (p<0.0001), and a higher percentage of males in group 2 (p<0.0001). No difference was seen with age, and weight, (p=0.294, p=0.625, respectively). There were more patients reported as Caucasian in group 2 (p=0.0001) and more reported as Caucasian/Hispanic in group 1 (p=0.0001). The rate of MetS between group 1 (54.45%) and group 2 (59.42%) was not statistically different (p = 0.427). Conclusion: No statistical difference was found in the rate of MetS between the two groups. Removing confounding drugs known to cause weight gain did not change these results.

No description available.