RESUMEN
Obesity in adolescents has been associated with increased cardiovascular risk factors such as dyslipidemia and insulin resistance. Several factors have been proposed to be associated with cardiovascular risk factors in adolescents including dietary habit, physical activity and genetic. This study was aimed to evaluate the interaction between genetic variation and dietary intake on cardiovascular metabolic risk factors in obese and normal weight adolescents. The UCP2 gene was chosen because it was previously correlated with dietary intake and cardiovascular risk factors. This study is a case control study done in 10 senior high school in Yogyakarta. Subjects were obese and normal weight adolescents taken from an obesity screening with age ranged between 16 and 18 years old. Dyslipidemia was observed by measuring total cholesterol, triglyceride, LDL dan HDL level while insulin resistance was determined by calculating fasting glucose and insulin level. Lipid profile, glucose and insulin level were measured after 8 hours of fasting. UCP2 -866G/A gene polymorphism were determined using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The results show that obese adolescents had significantly higher blood pressure, total cholesterol, LDL, triglyceride, insulin level and lower HDL level than their normal weight counterparts (all p<0.001). In obese adolescents, UCP2 -866G/A was associated with blood pressure (p=0.025), total cholesterol level (p=0.025), LDL (p=0.024) level and HOMA IR (p<0.001) but not with dietary fat intake (p=0.386). Additionally, subjects with UCP2 -866G/A gene polymorphism and high dietary fat intake had lower risk on obesity compared to those without UCP2 -866G/A gene polymorphism and low dietary fat intake. We conclude that the UCP2 -866G/A was associated with dyslipidemia, insulin resistance in obese adolescents. Additionally, we also observed the interaction between UCP2 -866G/A gene polymorphism and dietary intake on the risk of obesity.
RESUMEN
Estrogen has an important role in regulation of fat metabolism. Recent studies indicated that this process occurred due to inhibition of lipolysis by external estrogen administration. However, there was limited information regarding molecular process responsible for this phenomenon. This paper was aimed to present a brief update on recent studies explaining the effect of estrogen on adipose tissue lipolysis and the molecular pathway involved in this process. It is suggested that the effect of estrogen to reduction of lipolysis was through activation of estrogen receptor alpha (ER-α) in adipose tissue. This finding is supported by the fact that mice lacking of ESR1 gene (encodes ER-α) accumulate more fat and ESR1 mRNA in human adipose tissue was inversely correlated with body mass index (BMI). Future study should be aimed to clarify the role of ER-α on lipolysis in adipose tissue during weight loss intervention. Additionally, new pharmacological or nutritional treatment with ability to modulate ER-α activity/expression could be used as a potential weight loss intervention.