Altered control of cortisol secretion in adult men with low birth weight and cardiovascular risk factors
Altered control of cortisol secretion in adult men with low birth weight and cardiovascular risk factors
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DOI：
10.1210/jc.86.1.245
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发表时间：
2001-01-01
影响因子：
5.8
通讯作者：
Phillips, DIW
中科院分区：
文献类型：
--
作者：
Reynolds, RM;Walker, BR;Phillips, DIW
有研究表明，下丘脑-垂体-肾上腺轴的活动增加可能将低出生体重与随后的心血管危险因素和疾病的发展联系起来。205名男性，年龄66-77岁，出生并仍居住在东赫特福德郡，接受了过夜极低剂量（0.25 mg）地塞米松抑制试验，随后进行了低剂量1-mug ACTH-（1-24）刺激试验。收集24小时尿样，通过气相色谱/电子轰击质谱法分析皮质醇代谢产物。低出生体重的男性血浆皮质醇对ACTH-（1-24）的反应增强（P = 0.03），尿皮质醇代谢物总排泄量增加（调整高出生体重男性肥胖和瘦体重增加的混杂效应后; P = 0.04），但地塞米松治疗后血浆皮质醇无差异。代谢综合征的特征与肾上腺对ACTH-（1-24）的反应性增强（血压升高，P = 0.02;葡萄糖耐受不良，P = 0.09;高血糖症，P = 0.02）独立相关，有尿皮质醇代谢物排泄增加的趋势，但与地塞米松治疗后血浆皮质醇的差异无关。患有低出生体重和/或代谢综合征的男性下丘脑-垂体-肾上腺轴活动增加。这可能是一个重要的机制，支持早期生活中的事件对后来的心血管疾病的影响。
It has been suggested that increased activity of the hypothalamic-pituitary-adrenal axis may link low birth weight with subsequent development of cardiovascular risk factors and disease. Two hundred and five men, aged 66-77 yr, who were born and still live in East Hertfordshire underwent an overnight very low dose (0.25 mg) dexamethasone suppression test followed by a low dose 1-mug ACTH-(1-24) stimulation test. A 24-h urine sample was collected for analysis of cortisol metabolites by gas chromatography/electron impact mass spectrometry. Men with lower birth weight had enhanced responses of plasma cortisol to ACTH-(1-24) (P = 0.03), increased total urinary cortisol metabolite excretion (after adjustment for confounding effects of increased obesity and lean body mass in high birth weight men; P = 0.04), but no difference in plasma cortisol after dexamethasone. Features of the metabolic syndrome were independently associated with enhanced adrenal responsiveness to ACTH-(1-24) (raised blood pressure, P = 0.02; glucose intolerance, P = 0.09; hypertriglyceridemia, P = 0.02), with trends to increased urinary cortisol metabolite excretion, but not with differences in plasma cortisol after dexamethasone. Men with low birth weight and/or the metabolic syndrome have increased activity of the hypothalamic-pituitary-adrenal axis. This may be an important mechanism underpinning the effects of events in early life on later cardiovascular disease.