DYSFUNCTION OF PLACENTAL GLUCOCORTICOID BARRIER - LINK BETWEEN FETAL ENVIRONMENT AND ADULT HYPERTENSION
DYSFUNCTION OF PLACENTAL GLUCOCORTICOID BARRIER - LINK BETWEEN FETAL ENVIRONMENT AND ADULT HYPERTENSION
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DOI：
10.1016/0140-6736(93)90148-a
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发表时间：
1993-02-06
期刊：
影响因子：
168.9
通讯作者：
SECKL, JR
中科院分区：
文献类型：
--
作者：
EDWARDS, CRW;BENEDIKTSSON, R;SECKL, JR
低出生体重与成人生活常见疾病的后续发展有关，特别是高血压；母亲营养不良被认为是原因。我们建议另一种病因学--增加胎儿对母体糖皮质激素的暴露。这一假说得到了我们的发现的支持，即在大鼠中，作为母体糖皮质激素(11β-羟基类固醇脱氢酶)屏障的酶的活性降低与低出生体重有关。此外，胎儿对外源性糖皮质激素的暴露增加会导致出生体重降低，继而导致后代高血压。在产前发育的关键时期起作用的糖皮质激素，可能会像其他类固醇激素一样，发挥组织效应或印记一生持续的反应模式。因此，常见疾病的终生风险可能部分取决于宫内环境。
Low birthweight is associated with the subsequent development of common disorders of adult life, especially hypertension; maternal malnutrition has been suggested as the cause. We suggest an alternative aetiology-increased fetal exposure to maternal glucocorticoids. This hypothesis is supported by our findings that in rats decreased activity of the enzyme that acts as a placental barrier to maternal glucocorticoids (11beta-hydroxysteroid dehydrogenase) is associated with low birthweight. Furthermore, increased exposure of the fetus to exogenous glucocorticoids leads to low birthweight and subsequent hypertension in the offspring. Glucocorticoids acting during critical periods of prenatal development may, like other steroid hormones, exert organisational effects or imprint patterns of response that persist throughout life. Thus, the lifetime risk of common disorders may be partly determined by the intrauterine environment.