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血浆β-内啡肽的生理性升高会改变肥胖受试者而非正常体重受试者的葡萄糖代谢。

Physiological elevations of plasma beta-endorphin alter glucose metabolism in obese, but not normal-weight, subjects.

作者信息

Giugliano D, Cozzolino D, Salvatore T, Ceriello A, Torella R, Franchimont P, Lefebvre P J, D'Onofrio F

机构信息

Cattedra di Diabetologia, Prima Facoltà di Medicina, Università di Napoli, Italia.

出版信息

Metabolism. 1992 Feb;41(2):184-90. doi: 10.1016/0026-0495(92)90150-9.

DOI:10.1016/0026-0495(92)90150-9
PMID:1736041
Abstract

The present study was undertaken to evaluate the metabolic and hormonal responses to physiologic elevations of plasma beta-endorphin concentrations in both normal-weight and obese healthy subjects. The infusion of synthetic human beta-endorphin (4.5 ng/kg/min) produced the following: (1) in normal-weight subjects, no significant change of plasma glucose and pancreatic hormones (insulin, C-peptide, and glucagon), a significant plasma free fatty acids (FFA) increase, and a suppression of glycerol plasma levels; (2) in obese subjects, significant increases of glucose, insulin, C-peptide, and glucagon, a progressive decline of circulating FFA, and no change in glycerol plasma levels. In obese subjects, the intravenous administration of naloxone, given as a bolus (5 mg injected in 5 minutes) before the start of beta-endorphin infusion, reduced the plasma glucose response to the opioid by approximately half, annulled the pancreatic hormonal responses, and also reduced the FFA, but not glycerol, response. In normal-weight subjects, naloxone pretreatment did not induce any change of the flat glucose and hormonal responses to beta-endorphin, but reversed its effects on circulating FFA and glycerol. These data suggest that physiological elevations of plasma beta-endorphin concentrations produce metabolic and hormonal effects in obese subjects significantly different from those occurring in normal-weight subjects; these effects are partially naloxone-sensitive, suggesting the mediation of endogenous opioid receptors.

摘要

本研究旨在评估正常体重和肥胖健康受试者对血浆β-内啡肽浓度生理性升高的代谢和激素反应。输注合成人β-内啡肽(4.5 ng/kg/分钟)产生了以下结果:(1)在正常体重受试者中,血浆葡萄糖和胰腺激素(胰岛素、C肽和胰高血糖素)无显著变化,血浆游离脂肪酸(FFA)显著增加,甘油血浆水平受到抑制;(2)在肥胖受试者中,葡萄糖、胰岛素、C肽和胰高血糖素显著增加,循环FFA逐渐下降,甘油血浆水平无变化。在肥胖受试者中,在开始输注β-内啡肽前静脉推注纳洛酮(5分钟内注射5毫克),可使血浆葡萄糖对阿片类药物的反应降低约一半,消除胰腺激素反应,并降低FFA反应,但不降低甘油反应。在正常体重受试者中,纳洛酮预处理未引起对β-内啡肽的葡萄糖和激素反应的任何变化,但逆转了其对循环FFA和甘油的影响。这些数据表明,血浆β-内啡肽浓度的生理性升高在肥胖受试者中产生的代谢和激素效应与正常体重受试者显著不同;这些效应部分对纳洛酮敏感,提示内源性阿片受体的介导作用。

相似文献

1
Physiological elevations of plasma beta-endorphin alter glucose metabolism in obese, but not normal-weight, subjects.血浆β-内啡肽的生理性升高会改变肥胖受试者而非正常体重受试者的葡萄糖代谢。
Metabolism. 1992 Feb;41(2):184-90. doi: 10.1016/0026-0495(92)90150-9.
2
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Sensitivity to beta-endorphin as a cause of human obesity.
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Beta-endorphin-induced inhibition and stimulation of insulin secretion in normal humans is glucose dependent.β-内啡肽对正常人体胰岛素分泌的抑制和刺激作用取决于葡萄糖。
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Hyperglycemia and obesity as determinants of glucose, insulin, and glucagon responses to beta-endorphin in human diabetes mellitus.高血糖和肥胖作为人类糖尿病中葡萄糖、胰岛素和胰高血糖素对β-内啡肽反应的决定因素。
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Primary role of glucagon release in the effect of beta-endorphin on glucose homeostasis in normal man.在正常男性中,胰高血糖素释放在内啡肽对葡萄糖稳态影响中的主要作用。
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Beta-endorphin and islet hormone release in type-2 diabetes mellitus the effects of normoglycemia, enkephalin, naloxone and somatostatin.2型糖尿病中β-内啡肽与胰岛激素释放:血糖正常、脑啡肽、纳洛酮及生长抑素的作用
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Beta endorphin modulation of the glucoregulatory effects of repeated epinephrine infusion in alloxan-diabetic and normal dogs.β-内啡肽对四氧嘧啶糖尿病犬和正常犬重复输注肾上腺素的血糖调节作用的调节
Diabetologia. 1987 Sep;30(9):745-54. doi: 10.1007/BF00297000.

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Roles of β-Endorphin in Stress, Behavior, Neuroinflammation, and Brain Energy Metabolism.β-内啡肽在应激、行为、神经炎症和大脑能量代谢中的作用。
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