Krzyzanowska-Swiniarska B, Gruszczyńska M, Pilarska K, Widecka K, Czekalski S
Klinika Endokrynologii i Chorób Przemiany Materii Instytutu Chorób Wewnetrznych Pomorskiej AM, Szczecinie.
Endokrynol Pol. 1993;44(4):517-29.
The concentrations of beta-endorphin, ACTH, insulin (IRI), glucagon (IRG), cortisol and growth hormone were determined by radioimmunoassay during oral glucose tolerance test (OGTT) performed in 13 obese patients with normal glucose tolerance and without arterial hypertension. The test was performed in random, before and after intravenous administration of 0.8 mg of naloxone. Six persons with normal body weight served as controls. Higher basal concentrations of beta-endorphin and significant increase in beta-endorphin levels during OGTT, without concomitant increase in ACTH concentrations, have been found in obese patients. No effect of naloxone on beta-endorphin liberation during OGTT was observed, though the drug caused lowering in maximal increment of beta-endorphin and paradoxically lowered the concentrations of ACTH and cortisol. The basal concentrations of beta-endorphin did not correlate with the concentrations of insulin, ACTH, cortisol and growth hormone. Elevated concentrations of insulin, lowered concentration of growth hormone and normal levels of glucose and glucagon were observed in basal conditions, and excessive responses of insulin, glucose and glucagon were observed in obese patients during OGTT. Naloxone lowered insulin response and inhibited the fall of growth hormone during OGTT but did not influence the concentrations of glucose and glucagon. No correlation was found during OGTT after naloxone between insulin and beta-endorphin, ACTH or cortisol, whereas negative correlation was observed between insulin and growth hormone. The obtained results suggest that the elevated concentrations of beta-endorphin in simple obesity may be of both hypophyseal and peripheral origin. Hyper-beta-endorphinemia observed in obesity is probably not directly responsible for hyperinsulinemia, it may, however, be responsible for lower sensitivity of tissues to the action of insulin.
采用放射免疫分析法,对13例糖耐量正常且无动脉高血压的肥胖患者进行口服葡萄糖耐量试验(OGTT)期间,测定了β-内啡肽、促肾上腺皮质激素(ACTH)、胰岛素(IRI)、胰高血糖素(IRG)、皮质醇和生长激素的浓度。试验在随机状态下进行,于静脉注射0.8mg纳洛酮前后分别进行。6名体重正常者作为对照。在肥胖患者中发现,其基础β-内啡肽浓度较高,且在OGTT期间β-内啡肽水平显著升高,而ACTH浓度未随之升高。未观察到纳洛酮对OGTT期间β-内啡肽释放有影响,尽管该药物导致β-内啡肽最大增加值降低,且反常地降低了ACTH和皮质醇的浓度。β-内啡肽的基础浓度与胰岛素、ACTH、皮质醇和生长激素的浓度无相关性。在基础状态下观察到肥胖患者胰岛素浓度升高、生长激素浓度降低、血糖和胰高血糖素水平正常,且在OGTT期间胰岛素、血糖和胰高血糖素出现过度反应。纳洛酮降低了OGTT期间的胰岛素反应,并抑制了生长激素的下降,但未影响血糖和胰高血糖素的浓度。纳洛酮给药后,OGTT期间胰岛素与β-内啡肽、ACTH或皮质醇之间未发现相关性,而胰岛素与生长激素之间呈负相关。所得结果表明,单纯性肥胖中β-内啡肽浓度升高可能源于垂体和外周。肥胖中观察到的高β-内啡肽血症可能并非直接导致高胰岛素血症,然而,它可能是导致组织对胰岛素作用敏感性降低的原因。