Andrew R, Gale C R, Walker B R, Seckl J R, Martyn C N
Endocrinology Unit, Department of Medical Sciences, University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU.
Exp Clin Endocrinol Diabetes. 2002 Sep;110(6):284-90. doi: 10.1055/s-2002-34591.
The phenotype of the Metabolic Syndrome (hypertension, insulin resistance and hyperlipidaemia) bears similarities to Cushing's Syndrome, in which the cause of these features is elevated cortisol production. We have investigated relationships between glucocorticoid production and features of the Metabolic Syndrome in a cohort of elderly subjects.
A cross-sectional analysis was carried out of a subset of a birthweight cohort from Sheffield.
92 men and 40 women (aged 69-75 y) representative of the original cohort were investigated. Features of the Metabolic Syndrome (blood pressure, BMI, waist hip ratio, fasting glucose, insulin and triglycerides) were recorded and urinary glucocorticoid metabolites were measured by gas chromatography mass spectrometry.
Total glucocorticoid metabolites were correlated with the overall phenotype of the Metabolic Syndrome (P = 0.002), whereas specific pathways of metabolism (activity of 11 beta-hydroxysteroid dehydrogenases and A-ring reductases) did not show significant associations. Specifically total glucocorticoid production increased with increasing systolic blood pressure (r = 0.21, P = 0.013), fasting glucose (r = 0.19, P = 0.02) and insulin (r = 0.23, P = 0.025). Glucocorticoid production was greater with increasing abdominal girth (r = 0.19, P = 0.033), but there was no association with enhanced metabolism via a specific pathway. Within this cohort, birthweight was not associated with total glucocorticoid metabolites. However, decreasing birthweight (P = 0.022), increasing obesity (P = 0.026) and increasing total glucocorticoid production (P = 0.009) were all independent predictors of fasting glucose.
These data support the concept that cortisol production is enhanced in the Metabolic Syndrome, although they did not confirm the recent evidence that increased cortisol secretion is predicted by low birthweight.
代谢综合征（高血压、胰岛素抵抗和高脂血症）的表型与库欣综合征相似，在库欣综合征中，这些特征的病因是皮质醇分泌增加。我们在一组老年受试者中研究了糖皮质激素分泌与代谢综合征特征之间的关系。
对来自谢菲尔德的一个出生体重队列的一个子集进行横断面分析。
对92名男性和40名女性（年龄69 - 75岁）进行研究，这些受试者代表了原始队列。记录代谢综合征的特征（血压、体重指数、腰臀比、空腹血糖、胰岛素和甘油三酯），并通过气相色谱 - 质谱法测量尿糖皮质激素代谢产物。
总糖皮质激素代谢产物与代谢综合征的总体表型相关（P = 0.002），而特定的代谢途径（11β - 羟类固醇脱氢酶和A环还原酶的活性）未显示出显著相关性。具体而言，总糖皮质激素分泌随着收缩压升高（r = 0.21，P = 0.013）、空腹血糖升高（r = 0.19，P = 0.02）和胰岛素升高（r = 0.23，P = 0.025）而增加。糖皮质激素分泌随着腹围增加而增加（r = 0.19，P = 0.033），但与通过特定途径增强的代谢无关。在该队列中，出生体重与总糖皮质激素代谢产物无关。然而，出生体重降低（P = 0.022）、肥胖增加（P = 0.026）和总糖皮质激素分泌增加（P = 0.009）均是空腹血糖的独立预测因素。
这些数据支持了代谢综合征中皮质醇分泌增加的概念，尽管它们未证实近期低出生体重可预测皮质醇分泌增加的证据。
