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肥胖儿童对人促肾上腺皮质激素释放激素的β-内啡肽反应受损。

Impaired beta-endorphin response to human corticotropin-releasing hormone in obese children.

作者信息

Bernasconi S, Petraglia F, Iughetti L, Marcellini C, Lamborghini A, Facchinetti F, Genazzani A R

机构信息

Department of Pediatrics, University of Parma, Italy.

出版信息

Acta Endocrinol (Copenh). 1988 Sep;119(1):7-10. doi: 10.1530/acta.0.1190007.

Abstract

In order to evaluate the secretion of beta-endorphin in obese children and adolescents, we measured plasma beta-endorphin, ACTH and cortisol levels before and following administration of CRH (1 microgram/kg). Fourteen normal weight and 22 obese subjects (weight excess ranging from 30 to 98%) were studied. Plasma hormone levels were measured by radioimmunoassay directly in plasma (cortisol, ACTH) and after silicic acid extraction and Sephadex G-75 column chromatography (beta-endorphin). Basal beta-endorphin levels in obese children were significantly higher than in controls (14.7 +/- 1.8 vs 6.0 +/- 0.6 pmol/l; mean +/- SEM). No differences were found in basal ACTH and cortisol levels. CRH administration significantly increased beta-endorphin, ACTH and cortisol levels in normal subjects and ACTH and cortisol levels in obese subjects. Plasma beta-endorphin levels in obese children and adolescents did not show any significant increment. These data confirm the higher than normal beta-endorphin plasma levels in obese subjects in childhood and demonstrate that CRH is unable to increase beta-endorphin levels, suggesting an impairment of the hypothalamo-pituitary control mechanisms or an extra-anterior pituitary source.

摘要

为了评估肥胖儿童和青少年体内β-内啡肽的分泌情况,我们在给予促肾上腺皮质激素释放激素(CRH,1微克/千克)前后测量了血浆β-内啡肽、促肾上腺皮质激素(ACTH)和皮质醇水平。研究对象包括14名正常体重者和22名肥胖者(体重超重范围为30%至98%)。血浆激素水平通过放射免疫分析法直接检测血浆中的皮质醇和促肾上腺皮质激素,并在硅酸萃取和葡聚糖凝胶G-75柱层析后检测β-内啡肽。肥胖儿童的基础β-内啡肽水平显著高于对照组(分别为14.7±1.8与6.0±0.6皮摩尔/升;均值±标准误)。基础促肾上腺皮质激素和皮质醇水平未发现差异。给予CRH后,正常受试者的β-内啡肽、促肾上腺皮质激素和皮质醇水平以及肥胖受试者的促肾上腺皮质激素和皮质醇水平显著升高。肥胖儿童和青少年的血浆β-内啡肽水平未显示出任何显著升高。这些数据证实了肥胖儿童期受试者血浆β-内啡肽水平高于正常,并表明CRH无法升高β-内啡肽水平,提示下丘脑-垂体控制机制受损或存在垂体前叶以外的来源。

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