RESUMEN
Resumo Fundamento Foi demonstrado que o risco cardiometabólico está inversamente associado à aptidão cardiorrespiratória (APCR) e positivamente associado ao índice de massa corporal (IMC). Objetivo Analisar a associação de fatores de risco cardiometabólicos com IMC e APCR combinados em escolares de um município do sul do Brasil. Métodos Estudo transversal com uma amostra de 1252 escolares de sete a 17 anos. Foram avaliados colesterol total (CT), HDL-c, LDL-c, triglicerídeos (TG), pressão arterial sistólica (PAS) e diastólica (PAD). APCR e IMC foram agrupados em uma variável e os escolares classificados como eutróficos/aptos, eutróficos/inaptos, excesso de peso/aptos e excesso de peso/inaptos. Análises foram realizadas por meio de Regressão de Poisson e uma alfa de 0,05 foi adotado. Resultados Escolares classificados com excesso de peso/aptos demonstraram uma razão de prevalência (RP) de 1,50 (1,04 - 2,16) para TG alterado, 3,05 (2,05 - 4,54) para PAS e 2,70 (1,87 - 3,88) para PAD elevada. Escolares com excesso de peso/ inaptos apresentaram RP para CT alto de 1,24 (1,11 - 1,39) e 1,51 (1,11 - 2,04) para baixos níveis de HDL. Além disso, apresentaram um risco de 2,07 (1,60 - 2,69) para TG alterado, 3,26 (2,31 - 4,60) para PAS e 2,42 (1,76 - 3,32) para PAD elevada. Conclusão O IMC apresentou um papel central na associação com o risco e a APCR demonstrou atenuar a associação entre fatores de risco e excesso de peso. Escolares com excesso de peso apresentaram um risco cardiometabólico mais elevado, mas o tamanho do efeito foi maior entre os inaptos.
Abstract Background Cardiometabolic risk has been shown to be inversely associated with cardiorespiratory fitness (CRF) and positively associated with body mass index (BMI). Objective Our objective was to analyze the association of cardiometabolic risk factors with combined BMI and CRF in schoolchildren from a city in southern Brazil. Methods Cross-sectional study with a sample of 1252 schoolchildren aged seven to 17 years. Total cholesterol (TC), HDL-c, LDL-c, triglycerides (TG), systolic (SBP) and diastolic blood pressure (DBP) were evaluated. CRF and BMI were grouped into one variable and the schoolchildren were classified as eutrophic/fit, eutrophic/unfit, overweight-obese/fit, and overweight-obese/unfit. Crude and adjusted analyzes were performed using Poisson Regression and an alpha of 0.05 was adopted. Results Overweight-obese and fit schoolchildren showed a prevalence ratio (PR) of 1.50 (1.04 - 2.16) for altered TG, 3.05 (2.05 - 4.54) for elevated SBP, and 2.70 (1.87 - 3.88) for elevated DBP. Overweight-obese and unfit schoolchildren showed a PR for high TC of 1.24 (1.11 - 1.39) and 1.51(1.11 - 2.04) for low HDL levels. In addition, they had a risk of 2.07 (1.60 - 2.69) for altered TG, 3.36 (2.31 - 4.60) for elevated SBP and 2.42 (1.76 - 3.32) for altered DBP. Conclusion BMI played a central role in the association with risk and CRF was shown to attenuate the association between risk factors and obesity. Overweight-obese children and adolescents had a higher cardiometabolic risk, but the effect size was larger among the unfit.
RESUMEN
ABSTRACT The purpose of this study was to determine the effects of the high consumption of sucrose on the levels of DNA damage in blood, hippocampus and bone marrow of rats. Male Wistar rats were treated for 4 months with sucrose (10% for 60 initial days and 34% for the following 60 days) in drinking water, and then, glycemia and glycated hemoglobin (A1C) were measured. Levels of DNA damage in blood and hippocampus were evaluated by the comet assay. The micronucleus test was used to evaluate chromosomal damages in the bone marrow. The sucrose treatment significantly increased (p<0.01) the serum glucose levels (~20%) and A1C (~60%). The level of primary DNA damage was significantly increased (p<0.05) in hippocampal cells (~60%) but not in peripheral blood leukocytes (p>0.05). Additionally, it was observed a significative increase (p<0.05) in the markers of chromosomal breaks/losses in bone marrow, as indicated by the micronucleus test. This is the first study that evaluated DNA damage induced by high sucrose concentration in the hippocampus and bone marrow of rats. Sucrose-induced DNA damage was observed in both tissues. However, the mechanism of sucrose toxicity on DNA remains unknown.