RESUMO
ANTECEDENTES: Tanto el gen FTO (Fat-mass and obesity-associated-gene) y el tiempo sedente se asocian a obesidad, sin embargo, se desconoce si el tiempo sedente puede modificar la predisposición genética a la obesidad. Por ende, el objetivo de este estudio fue investigar si la asociación entre el polimorfismo rs9939609 del gen FTO y marcadores de adiposidad podrían ser modificados por el tiempo sedente. MÉTODOS: Este estudio de corte transversal incluye a 409 participantes del estudio GENADIO. Los marcadores de adiposidad estudiados fueron peso corporal, índice de masa corporal (IMC), perímetro de cintura (PC) y porcentaje masa grasa. El tiempo sedente se determinó mediante acelerometría de movimiento. La interacción entre el gen FTO (rs9939609) y el tiempo sedente sobre los marcadores de adiposidad se determinó mediante análisis de regresión múltiple. RESULTADOS: Tanto la variante de riesgo del gen FTO como el tiempo sedente se asociaron a mayor peso corporal, IMC, PC y masa grasa. Sin embargo, la asociación entre tiempo sedente y marcadores de adiposidad fue mayor en personas portadoras del alelo de riesgo del gen FTO. Por cada 1 hora de incremento en tiempo sedente, el peso corporal incrementa en 1,36 kg ([95% IC: 0,27; 2,46], p = 0,015) y 2,95 kg ([95% IC: 1,24; 4,65], p = 0,001) en personas con la variante protectora (TT) versus aquellos con la variante de riesgo (AA), respectivamente. Resultados similares se encontraron para (PC). CONCLUSIÓN: La asociación entre la variante de riesgo de FTO y mayor nivel de adiposidad es más acentuada en individuos que presentan mayores niveles de sedentarismo.
BACKGROUND: The Fat-mass and obesity-associated-gene (FTO gene) and sedentary behavior time are associated with obesity. However, whether sedentary behavior time can modify the genetic predisposition to obesity in the Chilean population is unknown. Therefore, this study investigated the association between sedentary behavior, adiposity markers, and the FTO gene. METHODS: This cross-sectional study included 409 participants from the Genes, Environment, Diabetes, and Obesity (GENADIO) study. Adiposity markers studied included body weight, body mass index (BMI), waist circumference (WC), and fat mass. Sedentary behaviors were measured using accelerometers. Using multiple regression, we evaluated the interaction between sedentary behaviors and the FTO gene (rs9939609) on adiposity markers. RESULTS: Sedentary behaviors and the FTO genotype were positively associated with higher body weight, BMI, WC, and fat mass. However, the association between time of sedentary behavior and adiposity markers was higher in carriers of the risk variant for the FTO gene. For each hour of increment in sedentary behaviors, body weight increases by 1.36 kg ([95% CI: 0.27; 2.46], p = 0.015) and 2.95 kg ([95%CI: 1.24; 4.65], p = 0.001) in non-risk carriers (TT) versus risk carriers (AA), respectively. We observed similar results for WC, BMI, and body fat, but the interaction was significant only for WC. CONCLUSION: The association between sedentary behaviors and adiposity markers, especially body weight and WC, is higher in individuals who carry the risk variant of the FTO gene.
Assuntos
Humanos , Masculino , Feminino , Adulto , Pessoa de Meia-Idade , Índice de Massa Corporal , Predisposição Genética para Doença/genética , Adiposidade/genética , Circunferência da Cintura/genética , Comportamento Sedentário , Dioxigenase FTO Dependente de alfa-Cetoglutarato/genética , Obesidade/genética , Chile , Estudos Transversais , Fatores de Risco , Polimorfismo de Nucleotídeo Único/genética , GenótipoRESUMO
BACKGROUND: The behavior of anthropometrics and the relationship with genetic factors through a long-term perspective should be better explored. This study aims to verify the odds of maintaining the nutritional status classification after three years, according to the rs9939609 polymorphism (FTO gene). METHODS: It was a retrospective longitudinal study with 355 schoolchildren (7-17 years). Body mass index, body-fat percentage (BF%), and waist circumference (WC) were measured at baseline and follow-up. The FTO gene was evaluated from blood collection and genotyping performed by real-time polymerase chain reaction. Odds ratios and 95% confidence intervals were calculated. RESULTS: For those homozygous with the A allele, the odds of being at less favorable classification at follow-up were 2.29 (1.24; 4.22) and 4.05 (2.08; 7.86) times higher than expected for BF% and WC, respectively, whereas the odds of being in the more favorable classification at follow-up were 0.34 (0.12; 0.93) and 0.11 (0.01; 0.78) for BF% and WC, respectively. The odds of being at less favorable classification were higher for AA carriers with less favorable classification at baseline for BF% and WC compared to AT and TT carriers. CONCLUSIONS: Schoolchildren with a genetic predisposition to obesity and unfavorable anthropometric profile at baseline had more chances of maintaining their nutritional status after three years of follow-up.
Assuntos
Adiposidade , Predisposição Genética para Doença , Humanos , Criança , Adiposidade/genética , Estudos Longitudinais , Estudos Retrospectivos , Obesidade/genética , Índice de Massa Corporal , Circunferência da Cintura/genética , Polimorfismo de Nucleotídeo Único , Dioxigenase FTO Dependente de alfa-Cetoglutarato/genéticaRESUMO
BACKGROUND: The Fat-mass and obesity-associated-gene (FTO gene) and sedentary behavior time are associated with obesity. However, whether sedentary behavior time can modify the genetic predisposition to obesity in the Chilean population is unknown. Therefore, this study investigated the association between sedentary behavior, adiposity markers, and the FTO gene. METHODS: This cross-sectional study included 409 participants from the Genes, Environment, Diabetes, and Obesity (GENADIO) study. Adiposity markers studied included body weight, body mass index (BMI), waist circumference (WC), and fat mass. Sedentary behaviors were measured using accelerometers. Using multiple regression, we evaluated the interaction between sedentary behaviors and the FTO gene (rs9939609) on adiposity markers. RESULTS: Sedentary behaviors and the FTO genotype were positively associated with higher body weight, BMI, WC, and fat mass. However, the association between time of sedentary behavior and adiposity markers was higher in carriers of the risk variant for the FTO gene. For each hour of increment in sedentary behaviors, body weight increases by 1.36 kg ([95% CI: 0.27; 2.46], p = 0.015) and 2.95 kg ([95%CI: 1.24; 4.65], p = 0.001) in non-risk carriers (TT) versus risk carriers (AA), respectively. We observed similar results for WC, BMI, and body fat, but the interaction was significant only for WC. CONCLUSION: The association between sedentary behaviors and adiposity markers, especially body weight and WC, is higher in individuals who carry the risk variant of the FTO gene.
Assuntos
Adiposidade , Dioxigenase FTO Dependente de alfa-Cetoglutarato , Índice de Massa Corporal , Predisposição Genética para Doença , Obesidade , Comportamento Sedentário , Circunferência da Cintura , Humanos , Dioxigenase FTO Dependente de alfa-Cetoglutarato/genética , Masculino , Feminino , Estudos Transversais , Chile , Adiposidade/genética , Adulto , Pessoa de Meia-Idade , Obesidade/genética , Circunferência da Cintura/genética , Predisposição Genética para Doença/genética , Genótipo , Fatores de Risco , Polimorfismo de Nucleotídeo Único/genéticaRESUMO
BACKGROUND: Genetic factors along with inadequate lifestyle habits are associated with the development of cardiometabolic alterations. Thus, the present study aimed to examine the role of sedentary behavior on the relationship between rs9939609 polymorphism (fat mass and obesity-associated gene-FTO) and cardiometabolic risk score according to cardiorespiratory fitness (CRF) levels in children and adolescents. METHODS: A cross-sectional study with 1215 children and adolescents (692 girls), aged between 6 and 17 years. Screen time as a marker of sedentary behavior was evaluated through a self-reported questionnaire and CRF was estimated using the 6-min walking and running test. The genotyping of the FTO rs9939609 polymorphism was performed using a real-time polymerase chain reaction. Clustered cardiometabolic risk score (cMetS) was calculated by summing z-scores of total cholesterol/high-density lipoprotein cholesterol ratio, triglycerides, glucose, systolic blood pressure, and waist circumference, and dividing it by five. Moderation analyses were tested using multiple linear regression models. RESULTS: The coefficient of the interaction term of FTO (rs9939609) and screen time indicated that screen time was a significant moderator on the relationship between FTO rs9939609 polymorphism and cMetS (p = 0.047) in children and adolescents classified with low CRF (ß = 0.001; 95% CI = 0.001; 0.002). It was observed a significant association between genotype risk (AA) of FTO polymorphism and cMetS, in participants that spent more than 378 min a day in front of screen-based devices (ß = 0.203; 95% CI = 0.000; 0.405). No interaction term was found for those with high CRF. CONCLUSIONS: High sedentary behavior seems to influence the relationship between genetic predisposition to obesity and cardiometabolic risk factors in children and adolescents with low CRF.
Assuntos
Aptidão Cardiorrespiratória , Doenças Cardiovasculares , Adolescente , Dioxigenase FTO Dependente de alfa-Cetoglutarato/genética , Índice de Massa Corporal , Doenças Cardiovasculares/diagnóstico , Doenças Cardiovasculares/genética , Criança , HDL-Colesterol , Estudos Transversais , Feminino , Predisposição Genética para Doença , Humanos , Masculino , Obesidade/complicações , Fatores de Risco , Comportamento Sedentário , Circunferência da Cintura/genéticaRESUMO
Leukocyte telomere length (LTL) is associated with obesity and may be involved in its aetiology, but few studies have focused on children and most have been cross-sectional. We assessed the relation of LTL with adiposity development in a prospective study of Colombian children. We quantified LTL at enrollment in 722 children aged 5-12 years and measured anthropometry annually for a median 6 years. Using mixed effects models, we estimated changes in adiposity measures including BMI and waist circumference (WC)-for-age z-scores in relation to baseline LTL z-score. In girls, longer LTL was linearly related to a lower increase in WC z-score from age 6 to 16 years. Every 1 SD LTL was associated with an adjusted 0.13 units lower increase in WC (95% CI: -0.23, -0.03; p = 0.01). In conclusion, longer LTL among girls in middle childhood is associated with smaller increases in WC, an indicator of abdominal adiposity.
Assuntos
Adiposidade , Obesidade , Telômero , Adiposidade/genética , Adolescente , Criança , Pré-Escolar , Colômbia , Estudos Transversais , Feminino , Humanos , Leucócitos , Masculino , Modelos Biológicos , Obesidade/genética , Estudos Prospectivos , Fatores Sexuais , Telômero/genética , Circunferência da Cintura/genéticaRESUMO
INTRODUCTION: Background: genetic variants of the FTO gene confer the highest risk of obesity identified so far. Associations between the FTO gene and alterations in metabolic markers have been reported in different populations but not in Chileans. The aim of this study was therefore to investigate the association of rs3751812 gene polymorphism with adiposity and metabolic markers in the Chilean adult population. Methods: genotype of the FTO gene was determined in 409 participants from the GENADIO study. Adiposity markers (body weight, BMI, % fat mass and waist circumference), metabolic markers (glycemia, insulin, HOMAIR, total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides, leptin, ALT, GGT, PCRhs) and blood pressure were measured. The association between the FTO genotype and the different markers was determined using linear regression analyses. Results: there was an association between the polymorphism and all adiposity markers as well as insulin, HOMAIR, leptin and HDL cholesterol (p < 0.05) in the fully adjusted model. For total cholesterol, triglycerides, LDL cholesterol, ALT, GGT and PCRhs, the association disappeared after adjustment by body mass index. Conclusion: our findings verify the association between the FTO rs3751812 polymorphism with obesity, hyperinsulinemia, hyperleptinemia and lower levels of HDL cholesterol in the Chilean population. These alterations could increase the risk of diabetes mellitus type II and metabolic syndrome.
INTRODUCCIÓN: Antecedentes: el gen FTO presenta las variantes genéticas que confieren el mayor riesgo de obesidad hasta ahora identificado. Se han reportado asociaciones de polimorfismos del gen FTO y alteraciones de marcadores metabólicos en diversas poblaciones, pero no en chilenos. El objetivo de este estudio fue investigar la asociación del polimorfismo rs3751812 con marcadores de adiposidad y metabólicos en adultos chilenos. Métodos: se determinó el genotipo del FTO en 409 participantes del estudio GENADIO. Se evaluaron marcadores de adiposidad (peso corporal, índice de masa corporal [IMC], % de masa grasa y perímetro de cintura), marcadores metabólicos (glicemia, insulina, HOMAIR, colesterol total, colesterol LDL, colesterol HDL, triglicéridos, leptina, ALT, GGT, PCRus) y presión arterial. La asociación entre el genotipo FTO y los distintos marcadores se realizó mediante análisis de regresión lineal. Resultados: tras ajustar los marcadores por las variables de confusión, se evidenció una asociación significativa de los genotipos de riesgo con todos los marcadores de adiposidad estudiados y con los marcadores metabólicos: insulina, HOMAIR, leptina y colesterol HDL (p < 0,05). Para colesterol total, triglicéridos, colesterol LDL, ALT, GGT y PCRus, la asociación perdió significancia al ajustar por IMC. Conclusión: este estudio revela que existe una asociación entre el polimorfismo rs3751812 del gen FTO con obesidad, hiperinsulinemia, hiperleptinemia y bajos niveles de colesterol HDL en la población chilena, lo que podría aumentar el riesgo de desarrollar diabetes mellitus tipo II y síndrome metabólico.
Assuntos
Adiposidade/genética , Dioxigenase FTO Dependente de alfa-Cetoglutarato/genética , Adulto , Biomarcadores/sangue , Índice de Massa Corporal , Peso Corporal , Chile/epidemiologia , Feminino , Frequência do Gene , Humanos , Masculino , Pessoa de Meia-Idade , Obesidade/epidemiologia , Obesidade/genética , Polimorfismo Genético , Fatores Socioeconômicos , Circunferência da Cintura/genética , Adulto JovemRESUMO
The prevalence of childhood obesity has increased worldwide. Although it is considered a polygenic inheritance disease, little is known about its susceptibility when the additive effect is considered. The aim of this study is to investigate whether the genetic risk score (GRS) based on previously associated obesity polymorphisms (SNP) rs9939609 (fat mass and obesity-associated (FTO)), rs6548238 (transmembrane protein 18 (TMEM18)) and rs16835198 (fibronectin type III domain containing 5 (FNDC5)) could serve as a predictor for anthropometric characteristics in a sample of Brazilian children and adolescents. This is a cross-sectional study with 1471 children and adolescents aged 6-17 years. BMI, waist circumference (WC) and percentage of body fat and metabolic parameters were verified. In all, three SNP were genotyped by TaqMan™ allelic discrimination. The metabolic and anthropometric parameters were compared between the genotypes, and the unweighted and weighted GRS (GRS and wGRS, respectively) were created to test the additive effect of these genetic polymorphisms on anthropometric parameters. The prevalence of overweight plus obesity was 41 %. Significant associations were identified for FTO rs9939609, TMEM18 rs6548238 and FNDC5 rs16835198 and for GRS and wGRS with anthropometric phenotypes. The higher score of wGRS was associated with obesity (OR: 2·65, 95 % CI 1·40, 5·04, P=0·003) and with greater WC (OR: 2·91, 95 % CI 1·57, 5·40, P=0·001). Our results suggest that these genetic variants contribute to obesity susceptibility in children and adolescents and reinforce the idea that the additive effect may be useful to elucidate the genetic component of obesity.
Assuntos
Dioxigenase FTO Dependente de alfa-Cetoglutarato/genética , Fibronectinas/genética , Predisposição Genética para Doença/genética , Proteínas de Membrana/genética , Obesidade Infantil/genética , Adolescente , Antropometria , Composição Corporal/genética , Índice de Massa Corporal , Brasil/epidemiologia , Criança , Feminino , Genótipo , Humanos , Masculino , Obesidade Infantil/epidemiologia , Polimorfismo de Nucleotídeo Único/genética , Circunferência da Cintura/genéticaRESUMO
Determinar la distribución genotípica y la frecuencia alélica del polimorfismo rs17817449 del gen FTO en jóvenes chilenos y su influencia en variables antropométricas. Los 96 sujetos jóvenes (18-25 años), 43 hombres y 53 mujeres fueron evaluados utilizando genotipificación del polimorfismo rs17817449 del gen FTO en TT, TG y GG mediante polimerase chain reaction (PCR), además de una evaluación Kinenatropométrica para determinar las variables asociadas a composición corporal. Las variables fueron analizadas estadísticamente según su distribución paramétrica y el nivel de significancia estadística fue p<0,05. La distribución genotípica del polimorfismo rs17817449 de FTO en jóvenes chilenos fue: TT: 50 %; TG: 42,7 %; GG 7,3 % y la distribución alélica fue: T: 0,7105 y G: 0,2895. No se encontraron diferencias estadísticamente significativas en las variables antropométricas al analizar los participantes según modelo de dominancia del alelo G. Se determinó la distribución genotípica y la frecuencia alélica del polimorfismo rs17817449 del gen FTO en jóvenes chilenos, datos desconocidos hasta este momento. De acuerdo a nuestros resultados, no existen diferencias antropométricas entre personas con diferentes genotipos del polimorfismo rs17817449 de FTO, agrupadas según modelo de dominancia del alelo G.
The rs17817449 polymorphism of the FTO gene in young Chileans and their influence on anthropometric variables. 96 young subjects (18-25 years old), 43 men and 53 women were evaluated using genotyping of the rs17817449 polymorphism of the FTO gene in TT, TG and GG by means of polymerase chain reaction (PCR), in addition to a Kinenatropometric evaluation to determine the variables associated with body composition. The variables were analyzed statistically according to their parametric distribution and the level of statistical significance was p<0.05. The genotypic distribution of the FTO polymorphism rs17817449 in young Chileans was: TT: 50 %; TG: 42.7 %; GG 7.3 % and the allelic distribution was: T: 0.7105 and G: 0.2895. No statistically significant differences were found in the anthropometric variables when analyzing the participants according to model of dominance of the G allele. The genotypic distribution and the allelic frequency of the rs17817449 polymorphism of the gene were determined FTO in Chilean population, data unknown until now. According to our results, there are no anthropometric differences between people with different genotypes of the FTO polymorphism rs17817449, nor according to the dominance model of the G.
Assuntos
Humanos , Masculino , Feminino , Adulto , Adulto Jovem , Antropometria , Polimorfismo de Nucleotídeo Único , Dioxigenase FTO Dependente de alfa-Cetoglutarato , Variação Genética , Índice de Massa Corporal , Chile , Reação em Cadeia da Polimerase , Adiposidade/genética , Circunferência da Cintura/genética , Frequência do Gene , GenótipoRESUMO
Knowledge on genetic and environmental (G × E) interaction effects on cardiometabolic risk factors (CMRFs) in children is limited. The purpose of this study was to examine the impact of G × E interaction effects on CMRFs in Mexican American (MA) children (n = 617, ages 6-17 years). The environments examined were sedentary activity (SA), assessed by recalls from "yesterday" (SAy) and "usually" (SAu) and physical fitness (PF) assessed by Harvard PF scores (HPFS). CMRF data included body mass index (BMI), waist circumference (WC), fat mass (FM), fasting insulin (FI), homeostasis model of assessment-insulin resistance (HOMA-IR), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG), systolic (SBP) and diastolic (DBP) blood pressure, and number of metabolic syndrome components (MSC). We examined potential G × E interaction in the phenotypic expression of CMRFs using variance component models and likelihood-based statistical inference. Significant G × SA interactions were identified for six CMRFs: BMI, WC, FI, HOMA-IR, MSC, and HDL, and significant G × HPFS interactions were observed for four CMRFs: BMI, WC, FM, and HOMA-IR. However, after correcting for multiple hypothesis testing, only WC × SAy, FM × SAy, and FI × SAu interactions became marginally significant. After correcting for multiple testing, most of CMRFs exhibited significant G × E interactions (Reduced G × E model vs. Constrained model). These findings provide evidence that genetic factors interact with SA and PF to influence variation in CMRFs, and underscore the need for better understanding of these relationships to develop strategies and interventions to effectively reduce or prevent cardiometabolic risk in children.
Assuntos
Doenças Cardiovasculares/genética , Interação Gene-Ambiente , Síndrome Metabólica/genética , Americanos Mexicanos/genética , Aptidão Física , Comportamento Sedentário , Adolescente , Glicemia/metabolismo , Índice de Massa Corporal , Criança , Feminino , Variação Genética , Humanos , Funções Verossimilhança , Masculino , Modelos Genéticos , Herança Multifatorial/genética , Fatores de Risco , Circunferência da Cintura/genéticaRESUMO
Polymorphisms in the LEP (G-2548A and A19G), LEPR (A326G, A668G and G3057A) and RETN (C-420G and G+62A) genes were documented according to their association with alterations in biochemical parameters such as glucose, insulin and lipid profiles, along with serum leptin and resistin concentrations. The aim of the study was to establish any contribution of the G-2548A and A19G polymorphisms of the LEP gene, the A326G, A668G and G3057A polymorphisms of the LEPR gene, and the C-420G and G+62A polymorphisms of the RETN gene to serum leptin and resistin levels in Mexican young adults. Clinical and biochemical variables, serum leptin and resistin levels, and genotype profiles were analysed in 66 Mexican young adults. Seven polymorphisms in the LEP, LEPR and RETN genes were genotyped using polymerase chain reaction-restriction fragment length polymorphisms analysis. Individuals carrying allele 3057A of the G3057A polymorphism in the LEPR gene showed significantly higher leptin concentrations than those bearing the genotype G/G (43.78 ± 39.11 vs 28.20 ± 14.12 ng/mL; p = 0.021). There were no associations of serum leptin or resistin levels according to the genotype of the other six analysed polymorphisms. Our results suggest that the allele 3057A of the LEPR G3057A polymorphism contributes to increased serum leptin levels in Mexican young adults.
Assuntos
Frequência do Gene , Leptina/genética , Polimorfismo de Nucleotídeo Único , Receptores para Leptina/genética , Resistina/genética , Adolescente , Adulto , Alelos , Distribuição da Gordura Corporal , Peso Corporal , Estudos Transversais , Feminino , Expressão Gênica , Genótipo , Humanos , Leptina/sangue , Masculino , México , Receptores para Leptina/sangue , Resistina/sangue , Estudantes , Circunferência da Cintura/genética , Relação Cintura-QuadrilRESUMO
Introduction. Increase in body weight is a gradual process that usually begins in childhood and in adolescence as a result of multiple interactions among environmental and genetic factors. This study aimed to analyze the relationship between copy number variants (CNVs) in five genes and four intergenic regions with obesity in Mexican children. Methods. We studied 1423 children aged 6-12 years. Anthropometric measurements and blood levels of biochemical parameters were obtained. Identification of CNVs was performed by real-time PCR. The effect of CNVs on obesity or body composition was assessed using regression models adjusted for age, gender, and family history of obesity. Results. Gains in copy numbers of LEPR and NEGR1 were associated with decreased body mass index (BMI), waist circumference (WC), and risk of abdominal obesity, whereas gain in ARHGEF4 and CPXCR1 and the intergenic regions 12q15c, 15q21.1a, and 22q11.21d and losses in INS were associated with increased BMI and WC. Conclusion. Our results indicate a possible contribution of CNVs in LEPR, NEGR1, ARHGEF4, and CPXCR1 and the intergenic regions 12q15c, 15q21.1a, and 22q11.21d to the development of obesity, particularly abdominal obesity in Mexican children.
Assuntos
Moléculas de Adesão Celular Neuronais/genética , Proteínas de Ligação a DNA/genética , Obesidade Abdominal/genética , Receptores para Leptina/genética , Composição Corporal/genética , Índice de Massa Corporal , Peso Corporal/genética , Criança , Variações do Número de Cópias de DNA/genética , DNA Intergênico/genética , Feminino , Proteínas Ligadas por GPI/genética , Estudos de Associação Genética , Predisposição Genética para Doença , Humanos , Masculino , México , Obesidade Abdominal/fisiopatologia , Fatores de Troca de Nucleotídeo Guanina Rho/genética , Circunferência da Cintura/genéticaRESUMO
Population admixture plays a role in the risk of chronic conditions that are related to body composition; however, our understanding of these associations in Puerto Ricans, a population characterized by multiple ancestries, is limited. This study investigated the relationship between genetic admixture and body composition in 652 Puerto Ricans from the Boston Puerto Rican Osteoporosis Study. Genetic ancestry was estimated from 100 ancestry-informative markers. Body composition measures were obtained from dual-energy X-ray absorptiometry. Multivariable linear regression analyses examined associations between bone mineral density (BMD) of the hip and lumbar spine and percent fat mass and lean mass with genetic admixture. In Puerto Ricans living on the US mainland, European ancestry was associated with lower BMD at the trochanter (P = 0.039) and femoral neck (P = 0.01), and Native American ancestry was associated with lower BMD of the trochanter (P = 0.04). African ancestry was associated with a higher BMD at the trochanter (P = 0.004) and femoral neck (P = 0.001). Ancestry was not associated with percent fat mass or lean mass or waist circumference. Our findings are consistent with existing research demonstrating inverse associations between European and Native American ancestries and BMD and positive relationships between African ancestry and BMD. This work contributes to our understanding of the high prevalence of chronic disease experienced by this population and has implications for other ethnic minority groups, particularly those with multiple ancestries. Future research should consider interactions between ancestry and environmental factors, as this may provide individualized approaches for disease prevention.
Assuntos
Composição Corporal/genética , Osteoporose/genética , Absorciometria de Fóton , Adiposidade/genética , Adulto , Densidade Óssea/genética , Osso e Ossos/diagnóstico por imagem , Osso e Ossos/fisiologia , Boston , Feminino , Estudos de Associação Genética , Hispânico ou Latino , Humanos , Masculino , Pessoa de Meia-Idade , Osteoporose/epidemiologia , Porto Rico , Circunferência da Cintura/genética , População Branca/genéticaRESUMO
BACKGROUND: There are different genetic patterns for cardio-metabolic parameters among different populations. Additionally, it has been found that ancestral genetic components (the proportion of Amerindian, European and African) in admixed Latin American populations influence an individual's susceptibility to cardio-metabolic disorders. The aim of this study was to evaluate the effect of ancestral genetic composition on a series of cardio-metabolic risk factors in a young admixed population from Colombia. RESULTS: In a sample of 853 Colombian youth, 10 to 18 years old, the mean European contribution was 66.6 % (range: 41-82 %), the mean African contribution was 14 % (range: 4-48 %), and the mean Amerindian contribution was 19.4 % (range: 10-35 %) using a panel of 40 autosomal ancestry-informative markers (AIMs). We assessed the degree of association between ancestral African, Amerindian and European genetic components and measures of body mass index, waist circumference, fasting glucose, fasting insulin, insulin resistance, triglycerides, high-density lipoprotein, and systolic and diastolic blood pressure. Two of the nine measures assessed presented a nominal significant association with ancestral components after adjusting for confounding variables: triglyceride levels were associated with the Amerindian component (OR = 1.06, 98.3 % CI = 1.01-1.11, P = 0.002) and systolic blood pressure was associated with the European component (OR = 0.93, 98.3 % CI = 0.87 to 0.99, P = 0.008) and the African component (OR = 1.07, CI = 1.01-1.14 P = 0.008), although it was not significant following a global Bonferroni correction. Additionally, insulin levels and insulin resistance showed associations with the African component. CONCLUSIONS: Our findings support the idea that an Amerindian ancestral component may act as a risk factor for high triglyceride levels. In addition, an African ancestral component confers a risk for high systolic blood pressure, and a European ancestry serves as a protective factor for this condition in a young admixed population from Colombia. However, these results should be confirmed in a larger population.
Assuntos
Predisposição Genética para Doença/genética , Miocárdio/metabolismo , Adolescente , Pressão Sanguínea/genética , Índice de Massa Corporal , Doenças Cardiovasculares/genética , Doenças Cardiovasculares/metabolismo , Criança , Colômbia/etnologia , Meio Ambiente , Feminino , Humanos , Insulina/metabolismo , Masculino , Fenótipo , Triglicerídeos/metabolismo , Circunferência da Cintura/genética , Adulto JovemRESUMO
BACKGROUND: There is growing interest in the hypertriglyceridemic waist (HTGW) phenotype, defined as high waist circumference (≥95 cm in males and ≥80 cm in females) combined with high serum triglyceride concentration (≥2.0 mmol/L in males and ≥1.5 mmol/L in females) as a marker of type 2 diabetes (T2D) and cardiovascular disease. However, the prevalence of this phenotype in high-risk populations, its association with T2D, and the genetic or epigenetic influences on HTGW are not well explored. Using data from large, extended families of Mexican Americans (a high-risk minority population in the USA) we aimed to: (1) estimate the prevalence of this phenotype, (2) test its association with T2D and related traits, and (3) dissect out the genetic and epigenetic associations with this phenotype using genome-wide and epigenome-wide studies, respectively. RESULTS: Data for this study was from 850 Mexican American participants (representing 39 families) recruited under the ongoing San Antonio Family Heart Study, 26 % of these individuals had HTGW. This phenotype was significantly heritable (h (2) r = 0.52, p = 1.1 × 10(-5)) and independently associated with T2D as well as fasting glucose levels and insulin resistance. We conducted genome-wide association analyses using 759,809 single nucleotide polymorphisms (SNPs) and epigenome-wide association analyses using 457,331 CpG sites. There was no evidence of any SNP associated with HTGW at the genome-wide level but two CpG sites (cg00574958 and cg17058475) in CPT1A and one CpG site (cg06500161) in ABCG1 were significantly associated with HTGW and remained significant after adjusting for the closely related components of metabolic syndrome. CPT1A holds a cardinal position in the metabolism of long-chain fatty acids while ABCG1 plays a role in triglyceride metabolism. CONCLUSIONS: Our results reemphasize the value of HTGW as a marker of T2D. This phenotype shows association with DNA methylation within CPT1A and ABCG1, genes involved in fatty acid and triglyceride metabolism. Our results underscore the importance of epigenetics in a clinically informative phenotype.
Assuntos
Epigênese Genética , Hipertrigliceridemia/genética , Americanos Mexicanos/genética , Circunferência da Cintura/genética , Membro 1 da Subfamília G de Transportadores de Cassetes de Ligação de ATP , Transportadores de Cassetes de Ligação de ATP/genética , Transportadores de Cassetes de Ligação de ATP/fisiologia , Carnitina O-Palmitoiltransferase/genética , Carnitina O-Palmitoiltransferase/fisiologia , Diabetes Mellitus Tipo 2/genética , Epigenômica , Família , Feminino , Marcadores Genéticos/genética , Estudo de Associação Genômica Ampla , Humanos , Masculino , Pessoa de Meia-Idade , Polimorfismo de Nucleotídeo ÚnicoRESUMO
AIMS: MicroRNAs (miRs) regulate processes involved in both cardiac remodeling and obesity. We investigated if the expression of selected miRs in patients with heart failure (HF) is influenced by the presence of obesity. METHODS: In this case-control study, we compared plasma levels of miR-21, -130b, -221, -423-5p, and the -221/-130b ratio in 57 age- and gender-matched subjects: 40 HF patients (20 obese HF and 20 lean HF) and 17 lean healthy controls. Body composition was estimated by bioelectrical impedance analysis. MiRs were measured by quantitative reverse transcription-PCR. Bioinformatics analysis was performed based on miRs findings to predict their putative targets and investigate their biological function. RESULTS: HF was associated with increased miR-423-5p levels in both lean and obese patients (P<0.05 vs. controls) without differences between HF groups. MiR-130b levels were reduced in obese HF patients compared with HF lean (P=0.036) and controls (P=0.025). MiR-221 levels were non-significantly increased in obese HF patients. MiR-21 levels were not different among the groups. MiR-221/-130b ratio was increased in obese HF patients, and was positively associated with body fat percentage (r=0.43; P=0.002), body mass index (r=0.44; P=0.002), and waist circumference (r=0.40; P=0.020). Computational prediction of target genes followed by functional enrichment analysis indicated a relevant role of miR-130b and miR-221 in modulating the expression of genes associated to cardiovascular and endocrine diseases, and suggested their influence in important signaling mechanisms and in numerous processes related to the circulatory and endocrine systems. CONCLUSIONS: In HF patients, the presence of obesity is associated with a differential expression of selected miRs and the miR-221/-130b ratio had significant correlations with adiposity parameters. Computational target prediction analysis identified several interrelated pathways targeted by miR-130b and miR-221 with a known relationship with endocrine and cardiovascular diseases, representing potential mechanisms to be further validated.
Assuntos
Insuficiência Cardíaca/sangue , Insuficiência Cardíaca/genética , MicroRNAs/sangue , Obesidade/sangue , Obesidade/genética , Magreza/sangue , Magreza/genética , Composição Corporal/genética , Índice de Massa Corporal , Estudos de Casos e Controles , Biologia Computacional/métodos , Feminino , Humanos , Masculino , MicroRNAs/genética , Pessoa de Meia-Idade , Circunferência da Cintura/genéticaRESUMO
AIMS: We aimed to determine the genetic and environmental correlation between various anthropometric indexes and incident Type 2 diabetes with a focus on waist circumference. METHODS: We used the data on extended Mexican-American families (808 subjects, 7617.92 person-years follow-up) from the San Antonio Family Heart Study and estimated the genetic and environmental correlations of 16 anthropometric indexes with the genetic liability of incident Type 2 diabetes. We performed bivariate trait analyses using the solar software package. RESULTS: All 16 anthropometric indexes were significantly heritable (range of heritabilities 0.24-0.99). Thirteen indexes were found to have significant environmental correlation with the liability of incident Type 2 diabetes. In contrast, only anthropometric indexes consisting of waist circumference (waist circumference, waist-hip ratio and waist-height ratio) were significantly genetically correlated (genetic correlation coefficients: 0.45, 0.55 and 0.44, respectively) with the liability of incident Type 2 diabetes. We did not observe such a correlation for BMI. CONCLUSIONS: Waist circumference as a predictor of future Type 2 diabetes is supported by the finding that they share common genetic influences.
Assuntos
Diabetes Mellitus Tipo 2/etnologia , Diabetes Mellitus Tipo 2/genética , Resistência à Insulina , Americanos Mexicanos/genética , Americanos Mexicanos/estatística & dados numéricos , Circunferência da Cintura , Adulto , Índice de Massa Corporal , Diabetes Mellitus Tipo 2/prevenção & controle , Feminino , Seguimentos , Humanos , Resistência à Insulina/etnologia , Resistência à Insulina/genética , Masculino , Pessoa de Meia-Idade , Valor Preditivo dos Testes , Prevalência , Estudos Prospectivos , Valores de Referência , Fatores de Risco , Estados Unidos/epidemiologia , Circunferência da Cintura/etnologia , Circunferência da Cintura/genéticaRESUMO
OBJECTIVE: The aim of the study was to investigate whether adiposity and metabolic markers, such as leptin, glucose, and lipids, are influenced by leptin (LEP) and leptin receptor (LEPR) gene polymorphisms in a sample of our population. SUBJECTS AND METHODS: A group of 326 individuals of Caucasian-European descent, aged 30 to 80 years, 87 men and 239 women, 148 obese and 178 non-obese, was randomly selected at two clinical hospitals in the city of Sao Paulo, Brazil. All individuals declared their ethnic group as white during the initial interview. Anthropometric measurements, body mass index (BMI), and fat mass were evaluated. Blood samples were drawn for DNA extraction and measurements of leptin, soluble leptin receptor, glucose, and lipids. LEP -2548G>A and LEPR Lys109Arg (c.326A>G), Gln233Arg (c.668A>G) and Lys656Asn (c.1968G>C) polymorphisms were detected by PCR-RFLP. RESULTS: Increased leptin and serum lipids, and LEPR Arg223Arg (GG genotype) were associated with higher risk for obesity (p < 0.05), while reduced risk was found in LEPR Arg109Arg (GG genotype) carriers (OR: 0.38, 95%CI: 0.19-0.77, p = 0.007). Multiple linear regression analysis showed a relationship between LEPR 223Arg, increased waist circumference, and leptinemia (p < 0.05), while LEPR 109Arg was associated with high total cholesterol and triglycerides (p < 0.05). LEPR haplotype 3 (AGG: 109Lys/233Arg/656Lys) carriers have increased risk for obesity (OR: 2.56, 95% CI: 1.19-5.49, p = 0.017). Moreover, this haplotype was associated with increased BMI, waist circumference, and leptinemia (p < 0.05). CONCLUSIONS: LEPR polymorphisms are associated with obesity, hyperleptinemia, and atherogenic lipid profile, suggesting their potential role for leptin resistance and cardiovascular risk. Moreover, LEPR haplotype 3 confers susceptibility to adiposity and hyperleptinemia in our population.
OBJETIVO: O estudo teve por objetivo investigar a influência de polimorfismos nos genes da leptina (LEP) e do receptor de leptina (LEPR) na adiposidade e em marcadores metabólicos, como leptina, glicose e lipídeos, em uma amostra de nossa população. SUJEITOS E MÉTODOS: Um grupo de 326 indivíduos com idade de 30 a 80 anos, 87 homens e 239 mulheres, 148 obesos e 178 não obesos, e de etnia branca foi selecionado aleatoriamente em dois hospitais clínicos da cidade de São Paulo, Brasil. Medidas antropométricas, índice de massa corporal (IMC) e gordura corporal foram avaliados. Amostras de sangue foram obtidas para extração de DNA e determinações de leptina, receptor de leptina solúvel, glicose e lipídeos. Os polimorfismos LEP -2548G>A e LEPR Lys109Arg (c.326A>G), Gln233Arg (c.668A>G) e Lys656Asn (c.1968G>C) foram detectados por PCR-RFLP. RESULTADOS: Leptina e lipídeos séricos aumentados e LEPR Arg223Arg (genótipo GG) foram associados com maior risco de obesidade (p < 0,05), enquanto foi encontrado risco reduzido de obesidade, em portadores de LEPR Arg109Arg (genótipo GG) (OR: 0,38, 95%CI: 0,19-0,77, p = 0,007). A análise de regressão linear múltipla mostrou relação entre o alelo LEPR 223Arg e circunferência abdominal e leptinemia aumentadas (p < 0,05), enquanto o alelo LEPR 109Arg foi associado com aumento de colesterol total e triglicerídeos (p < 0,05). Os portadores do haplotipo 3 do LEPR (AGG: 109Lys/233Arg/656Lys) tiveram maior risco aumentado para obesidade (OR: 2.56, 95% CI: 1.19-5.49, p = 0,017). Além disso, esse haplótipo foi associado com IMC, circunferência abdominal e leptinemia aumentados (p < 0,05). CONCLUSÕES: Polimorfismos de LEPR são associados com obesidade, hiperleptinemia e perfil lipídico aterogênico sugerindo seu papel potencial para a resistência à leptina e risco cardiovascular.
Assuntos
Adulto , Idoso , Idoso de 80 Anos ou mais , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Adiposidade/genética , Leptina/genética , Obesidade/genética , Polimorfismo de Fragmento de Restrição/genética , Receptores para Leptina/genética , Análise de Variância , Brasil , Biomarcadores/sangue , Glicemia/metabolismo , Distribuição de Qui-Quadrado , Frequência do Gene , Glucose/metabolismo , Leptina/sangue , Obesidade/sangue , Reação em Cadeia da Polimerase , Fatores de Risco , Receptores para Leptina/sangue , Circunferência da Cintura/genéticaRESUMO
OBJECTIVE: The aim of the study was to investigate whether adiposity and metabolic markers, such as leptin, glucose, and lipids, are influenced by leptin (LEP) and leptin receptor (LEPR) gene polymorphisms in a sample of our population. SUBJECTS AND METHODS: A group of 326 individuals of Caucasian-European descent, aged 30 to 80 years, 87 men and 239 women, 148 obese and 178 non-obese, was randomly selected at two clinical hospitals in the city of Sao Paulo, Brazil. All individuals declared their ethnic group as white during the initial interview. Anthropometric measurements, body mass index (BMI), and fat mass were evaluated. Blood samples were drawn for DNA extraction and measurements of leptin, soluble leptin receptor, glucose, and lipids. LEP -2548G>A and LEPR Lys109Arg (c.326A>G), Gln233Arg (c.668A>G) and Lys656Asn (c.1968G>C) polymorphisms were detected by PCR-RFLP. RESULTS: Increased leptin and serum lipids, and LEPR Arg223Arg (GG genotype) were associated with higher risk for obesity (p < 0.05), while reduced risk was found in LEPR Arg109Arg (GG genotype) carriers (OR: 0.38, 95%CI: 0.19-0.77, p = 0.007). Multiple linear regression analysis showed a relationship between LEPR 223Arg, increased waist circumference, and leptinemia (p < 0.05), while LEPR 109Arg was associated with high total cholesterol and triglycerides (p < 0.05). LEPR haplotype 3 (AGG: 109Lys/233Arg/656Lys) carriers have increased risk for obesity (OR: 2.56, 95% CI: 1.19-5.49, p = 0.017). Moreover, this haplotype was associated with increased BMI, waist circumference, and leptinemia (p < 0.05). CONCLUSIONS: LEPR polymorphisms are associated with obesity, hyperleptinemia, and atherogenic lipid profile, suggesting their potential role for leptin resistance and cardiovascular risk. Moreover, LEPR haplotype 3 confers susceptibility to adiposity and hyperleptinemia in our population.
Assuntos
Adiposidade/genética , Leptina/genética , Obesidade/genética , Polimorfismo de Fragmento de Restrição/genética , Receptores para Leptina/genética , Adulto , Idoso , Idoso de 80 Anos ou mais , Análise de Variância , Biomarcadores/sangue , Glicemia/metabolismo , Brasil , Distribuição de Qui-Quadrado , Feminino , Frequência do Gene , Glucose/metabolismo , Humanos , Leptina/sangue , Masculino , Pessoa de Meia-Idade , Obesidade/sangue , Reação em Cadeia da Polimerase , Receptores para Leptina/sangue , Fatores de Risco , Circunferência da Cintura/genéticaRESUMO
BACKGROUND: CAH patients have an increased risk of cardiovascular disease, and it remains unknown if lifelong glucocorticoid (GC) treatment is a contributing factor. In the general population, glucocorticoid receptor gene (NR3C1) polymorphisms are associated with an adverse metabolic profile. Our aim was to analyze the association between the NR3C1 polymorphisms and the metabolic profile of CAH patients. METHODOLOGY: Sixty-eight adult patients (34SV/34SW) with a mean age of 28.4±9 years received dexamethasone (mean 0.27±0.11 mg/day) to obtain normal androgen levels. SW patients also received fludrocortisone (50 µg/day). Metabolic syndrome (MetS) was defined by the NCEP ATPIII criteria and obesity by BMI ≥30 kg/m². NR3C1 alleles were genotyped, and association analyses with phenotype were carried out with Chi-square, t-test and regression analysis. RESULTS: Obesity and MetS were observed in 23.5% and 7.3% of patients, respectively, and were not correlated with GC doses and treatment duration. BMI was positively correlated with blood pressure (BP), triglycerides (TG), LDL-c levels and HOMA-IR and inversely correlated with HDL-c levels. BclI and A3669G variants were found in 26.4% and 9.6% of alleles, respectively. Heterozygotes for the BclI polymorphism presented with higher BMI (29 kg/m²±5.3 vs. 26 kg/m²±5.3, respectively) and waist circumference (89 cm±12.7 vs. 81 cm±13, respectively) compared to wild-type subjects. Hypertension was found in 12% of patients and heterozygotes for the BclI polymorphism presented higher systolic BP than wild type subjects. Low HDL-c and high TG levels were identified in 30% and 10% of patients, respectively, and were not associated with the NR3C1 polymorphisms. A3669G carriers and non-carriers did not differ. CONCLUSION: In addition to GC therapy, the BclI GR variant might play an important role in obesity susceptibility in CAH patients. Genotyping of GR polymorphisms could result in the identification of a subgroup at risk patients, allowing for the establishment of personalized treatment and the avoidance of long-term adverse consequences.
Assuntos
Hiperplasia Suprarrenal Congênita/genética , Hiperplasia Suprarrenal Congênita/metabolismo , Metaboloma/genética , Polimorfismo Genético , Receptores de Glucocorticoides/genética , Hiperplasia Suprarrenal Congênita/complicações , Hiperplasia Suprarrenal Congênita/fisiopatologia , Adulto , Biomarcadores/metabolismo , Pressão Sanguínea/genética , Índice de Massa Corporal , Feminino , Heterozigoto , Humanos , Masculino , Síndrome Metabólica/complicações , Obesidade/complicações , Circunferência da Cintura/genéticaRESUMO
Objetivo: comparar las mediciones de perímetro cintura e índice cintura-cadera para determinar la frecuencia del síndrome metabólico en familiares de primer grado de personas con diabetes tipo 1, utilizando diferentes definiciones pediátricas. Métodos: se estudiaron 224 familiares de primer grado de personas con diabetes tipo 1, en edades comprendidas entre los 4 y los 19 años. Se les determinó peso, talla, perímetro cintura y perímetro cadera, tensión arterial, glucemia, triglicéridos y HDL-colesterol. Se aplicaron las definiciones de síndrome metabólico según los criterios de Cook, Ford, la Federación Internacional de Diabetes y del consenso cubano. Se realizó una variante del consenso cubano utilizando: índice de masa corporal e índice cintura-cadera, según tablas cubanas, valores de glucosa ³ 5,6 mmol/L y tensión arterial ³ 90 percentil (tablas cubanas). Se tomaron, de forma independiente, los criterios de HDL-colesterol y triglicéridos. Empleamos el índice cintura-cadera de las tablas cubanas, el perímetro cintura sugerido por la Asociación Latinoamericana de Diabetes y el europeo para las definiciones estudiadas. Para la comparación de las frecuencias del síndrome metabólico, se usó la prueba exacta de Fisher. Resultados: la frecuencia del síndrome metabólico al aplicar la variante del consenso cubano fue de 9,37 por ciento (21/224). Al comparar la variante del consenso cubano con las definiciones de Cook, Ford y la Federación Internacional de Diabetes (que utiliza el perímetro cintura de la Asociación Latinoamericana de Diabetes), se observó diferencia significativa con Cook y la Federación Internacional de Diabetes (4,01 por ciento, p= 0,0360; 1,33 por ciento, p= 0,0002 respectivamente). Al confrontar la presencia del síndrome metabólico de la variante del consenso cubano con Cook (8,48 por ciento; 19/224) y Ford (8,93 por ciento; 20/224), teniendo en cuenta el índice cintura-cadera de las tablas cubanas, podemos detectar frecuencias similares de familiares de primer grado de personas con diabetes tipo 1 con síndrome metabólico. En cambio, encontramos diferencias significativas cuando comparamos las frecuencias del síndrome metabólico de la variante del consenso cubano (p= 0,0019), de Cook (p= 0,0053) y de Ford (p= 0,0032), con la definición sugerida por la Federación Internacional de Diabetes (2,23 pr ciento; 5/224) empleando el índice cintura-cadera. Conclusiones: nuestros datos indican que para el diagnóstico del síndrome metabólico debemos utilizar el índice cintura-cadera y no el perímetro cintura sugerido por la Asociación Latinoamericana de Diabetes, aún sin presentar datos propios del perímetro cintura de la población cubana(AU)
Objective: to compare the measurements of waist circumference and waist-hip circumference to determine the frequency of metabolic syndrome in first degree relatives of persons with type 1diabetes, using different pediatric definitions. Methods: two hundred twenty four first degree relatives of persons with type 1 diabetes were studied in ages from 4 to 10 years. Weight, height, waist-hip circumference, blood pressure, glycemia, triglycerides and HDL-cholesterol were determined. The definitions of metabolic syndrome according to Cook, Ford, International Federation of Diabetes and the Cuban consensus were applied. A variant of Cuban consensus was performed using: body mass index and waist-hip index according the Cuban tables, values of glucose ³ 5,6 mmol/L and blood pressure ³ 90 percentile (Cuban tables). In an independent way, criteria of HDL-cholesterol and triglycerides were taken into account. The waist-hip index of Cuban tables, the waist circumference suggested by the Latin-American and European Association of Diabetes for study definitions were applied. For comparison of frequencies of metabolic syndrome the Fisher exact test was used. Results: the frequency of metabolic syndrome with application of Cuban consensus variant was of 9,37 percent (21/224). Comparing the above variant with the definitions of Cook, Ford and of the International Federation of Diabetes (using the waist circumference of the Latin-American Association of Diabetes, there was a significant difference between Cook and the International Federation of Diabetes (4,01 percent, p= 0,0360; 1,33 percent, p= 0,0002, respectively). Comparing the presence of metabolic syndrome of the Cuban consensus variant with Cook (8,48 percent; 19/224) and Ford (8,93 percent; 20/224) taking into account the waist-hip index of the Cuban tables, it is possible to detect similar frequencies of first degree relatives of persons with type 1 diabetes with metabolic syndrome. On the other hand, we found significant differences comparing the frequencies of metabolic syndrome of the Cuban consensus variant (p= 0,0019), of Cook (p= 0,0053) and of Ford (p= 0,0032) with the definition suggested by the International Federation of Diabetes (2,23 percent; 5/224) using the waist-hip index. Conclusions: our data demonstrate that for the diagnosis of metabolic syndrome we must to use the waist-hip index and not the circumference suggested by the Latin-American Association of Diabetes, still without to present own data of waist-hip circumference of the Cuban population(AU)