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Perinatal Programming of Central Obesity and the Metabolic Syndrome: Role of Glucocorticoids

机译:围产期编程的中央肥胖和代谢综合症:糖皮质激素的作用。

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摘要

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 glucocorti-coids 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 in-creased local glucocorticoid exposure and sensitivity. In addition to an improvement of the health of pregnant women, early diagnosis of metabolic and hormonal disturbances is impor-tant 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 conse-quences of hypercorticism.
机译:宫内生长迟缓(IUGR)与成年后中央肥胖,代谢综合征及其并发症(2型糖尿病和冠心病)的患病率增加有关。促肾上腺皮质功能的编程是上述现象的基础机制之一。从母亲到胎儿的活性糖皮质激素增加的传递,可以在中枢神经系统水平上发挥作用,以增强对应激的反应,而在外周水平上,可以在脂肪组织中引起局部糖皮质激素暴露的增加和敏感性。 IUGR儿童除了改善孕妇健康外,还必须早期诊断代谢和激素紊乱,以防止代偿性补充生长及其随后的肥胖,并建立治疗干预措施反对高皮质主义的有害后果。

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