Perinatal programming of central obesity and the metabolic syndrome: Role of glucocorticoids
Perinatal programming of central obesity and the metabolic syndrome: Role of glucocorticoids
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DOI：
10.1089/met.2006.4.129
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发表时间：
2006-06-01
影响因子：
2.1
通讯作者：
Grino, Michel
中科院分区：
文献类型：
--
作者：
Achard, Vincent;Boullu-Ciocca, Sandrine;Grino, Michel
宫内生长迟缓（IUGR）与成人中枢性肥胖、代谢综合征及其并发症（2型糖尿病和冠心病）患病率增加有关。促皮质功能的程序化是上述现象背后的机制之一。活跃的糖皮质激素从母体传递到胎儿的通道增加，在中枢神经系统水平上，可以增强对压力的反应，在外周水平上，脂肪组织可以诱导局部糖皮质激素暴露和敏感性的增加。除了改善孕妇的健康外，对IUGR儿童的代谢和激素紊乱的早期诊断也很重要，以防止代偿性追赶生长及其随后的肥胖，并针对过度皮质的有害后果制定治疗干预措施。
Intrauterine growth retardation (IUGR) is associated with increased prevalence, at the adult age, of central obesity, the metabolic syndrome, and its complications (type 2 diabetes and coronary heart disease). Programming of the corticotropic function is one of the mechanisms underlying the above-mentioned phenomenon. An increased passage of active glucocorticoids from the mother to the fetus can act, at the central nervous system level, to program an enhanced response to stress and, at the peripheral level, in adipose tissue to induce an increased local glucocorticoid exposure and sensitivity. In addition to an improvement of the health of pregnant women, early diagnosis of metabolic and hormonal disturbances is important in children with IUGR, in order to prevent a compensatory catch-up growth and its subsequent obesity, and to set up a therapeutic intervention against the deleterious consequences of hypercorticism.