Relationship between lifestyle-related diseases in childhood and the risk for atherosclerotic coronary heart disease in adulthood (studies on lipoprotein abnormality, adipocytokine, vascular endothelial function and related genes)

许多研究表明，生活方式相关的疾病是动脉粥样硬化性冠心病(ACHD)的危险因素。病理性动脉硬化病变存在于儿童中，即使在儿童中也很可能随着生活方式相关疾病的存在而加速动脉粥样硬化病变的发展。因此，在本研究中，我们研究了学龄儿童和新生儿体重与血清脂肪细胞因子浓度的关系。在学龄儿童中，除脂联素外，所有脂肪细胞因子(脂联素、瘦素、IL-6、IL-18、IL-1β)均与体重呈正相关。脂联素与体重呈负相关，这些发现与成人相似，从而表明超重是ACHD的危险因素，即使在儿童中也是如此。与学龄儿童不同，早产儿和足月儿的血清脂联素浓度与体重呈正相关。到目前为止，…的一些角色在成人中，更多的脂肪细胞因子，如IL-6和肿瘤坏死因子-α，在脂联素与体重的负相关中被强调。已有研究表明，IL-6和肿瘤坏死因子-α可减少脂肪细胞分泌脂联素。脂肪组织中的某些炎症可能是导致脂联素与体重负相关的原因之一。如果脂肪组织中的炎症或促炎脂肪细胞因子水平没有增加，脂肪细胞的脂联素分泌可能不会减少。由于妊娠晚期胎儿体重的增加是一种生理发育，因此有理由认为，在这个阶段脂肪组织的增加可能不会伴随脂肪组织的炎症。此外，早产儿高分子脂联素(活性脂联素)占总脂联素的比例明显低于足月儿。由于脂联素是由脂肪细胞分泌的，我们的发现提示早产儿脂肪组织的发育可能与足月儿不同。这可能解释了低出生体重儿与ACHD未来发展的关系。较少

Many studies have shown that life-style related disorders are risk factors for atherosclerotic coronary heart diseases (ACHD). The pathological arterial sclerosis lesion is present in children, and it is very likely that the development of atherosclerotic lesion is accelerated with the presence of life-style related diseases even in children. Thus, in the present study, we studied the relationship between body weight and serum concentrations of adipocytokines in school children and neonates. In schoolchildren, all adipocytokines evaluated (adiponectin, leptin, Il-6, IL-18, IL-1β) were positively correlated with body weight except for adiponectin. Adiponectin was inversely correlated with body weight These findings were similar to those in adults, thereby suggesting that overweight was a risk factor for ACHD even in children. Differed from school children, serum concentrations of adiponectin were positively associated with body weight in preterm and term infants. To date, some roles of … More adipocytokines such as IL-6 and TNF-α have been highlighted in the inverse correlation between adiponectin and body weight in adults. It has been shown that IL-6 and TNF-α reduce the secretion of adiponectin from adipocytes. Some kinds of inflammation in adipose tissue might contribute to the inverse correlation between adiponectin and body weight. If inflammation or levels of pro-inflammatory adipocytokines were not elevated in adipose tissue, adiponectin secretion from adipocytes might not be reduced. Since the increase in the body weight of the fetus during late pregnancy is a physiological development, it is reasonable to consider that an increase in adipose tissue at this stage might not accompany the inflammation in adipose tissue. Furthermore, the ratio of high-molecular adiponectin (active adiponectin) to total adiponectin was significantly smaller in preterm infant that that in term infant. As adiponectin was secreted from adipocytes, our findings suggest that development of adipose tissue in preterm infants might be different from term infant. This may explain the relation of low birth weight to future development of ACHD. Less