Nakai Y, Hamagaki S, Takagi R, Taniguchi A, Kurimoto F
College of Medical Technology, Kyoto University, Japan.
Clin Endocrinol (Oxf). 2000 Sep;53(3):383-8. doi: 10.1046/j.1365-2265.2000.01091.x.
Tumor necrosis factor-alpha (TNF-alpha) is a cytokine with numerous immunological and metabolic activities. In addition, TNF-alpha can stimulate a variety of physiological, neuroendocrine and behavioural responses of the central nervous system. In experimental animals, TNF-alpha induces changes in physiological and behavioural parameters which have also been observed in eating disorders. The biological activities of TNF-alpha are mediated by two structurally related, but functionally distinct receptors, TNF-RI and TNF-RII. Since injection of TNF-alpha results in increased shedding of TNF-alpha receptors, it is likely that TNF-alpha release is reflected by soluble TNF-receptors (sTNF-Rs) levels.
We studied plasma concentrations of TNF-alpha and two sTNF-Rs (sTNF-RI and sTNF-RII) in female patients with bulimia nervosa.
Twenty female patients with bulimia nervosa (BN) and 20 age-matched normal women (N) were studied.
Plasma TNF-alpha concentrations were measured by enzyme immunoassay kit and plasma concentrations of sTNF-RI and sTNF-RII were measured by enzyme-linked immunosorbent assay.
Plasma TNF-alpha concentrations in BN were significantly higher than those in N (4.7+/- 0.5 ng/l vs. 1.6+/-0.1 ng/l; P<0.01). Although no significant difference was observed in plasma sTNF-RI concentrations between the two groups, plasma sTNF-RII concentrations in BN were significantly higher than those in N (2080.0+/-107.5 ng/l vs. 1569.5 +/-84.0 ng/l; P<0.01). Plasma TNF-alpha concentrations were significantly related to plasma sTNF-RI concentrations (r = 0.511, P<0.05) and to plasma sTNF-RII concentrations (r = 0.532, P<0.05) in bulimic patients. However, plasma TNF-alpha concentrations were not related to body fat mass or to bulimic behaviours in these patients.
Our present findings suggest that the adipose tissue may not be the immediate source of TNF-alpha in bulimic patients but the increase in plasma TNF-alpha in these patients may be derived from the central nervous system sources. The elevated sTNF-RII may reflect different shedding kinetics compared with sTNF-RI in bulimic patients.
肿瘤坏死因子-α(TNF-α)是一种具有多种免疫和代谢活性的细胞因子。此外,TNF-α可刺激中枢神经系统的多种生理、神经内分泌和行为反应。在实验动物中,TNF-α可诱导生理和行为参数的变化,这些变化在饮食失调中也有观察到。TNF-α的生物学活性由两种结构相关但功能不同的受体介导,即TNF-RI和TNF-RII。由于注射TNF-α会导致TNF-α受体的脱落增加,因此可溶性TNF受体(sTNF-Rs)水平可能反映了TNF-α的释放。
我们研究了神经性贪食症女性患者血浆中TNF-α和两种sTNF-Rs(sTNF-RI和sTNF-RII)的浓度。
研究了20名神经性贪食症(BN)女性患者和20名年龄匹配的正常女性(N)。
采用酶免疫分析试剂盒测定血浆TNF-α浓度,采用酶联免疫吸附测定法测定血浆sTNF-RI和sTNF-RII浓度。
BN患者血浆TNF-α浓度显著高于N组(4.7±0.5 ng/l对1.6±0.1 ng/l;P<0.01)。虽然两组之间血浆sTNF-RI浓度未观察到显著差异,但BN患者血浆sTNF-RII浓度显著高于N组(2080.0±107.5 ng/l对1569.5±84.0 ng/l;P<0.01)。在贪食症患者中,血浆TNF-α浓度与血浆sTNF-RI浓度显著相关(r = 0.511,P<0.05),与血浆sTNF-RII浓度也显著相关(r = 0.532,P<0.05)。然而,这些患者的血浆TNF-α浓度与体脂量或贪食行为无关。
我们目前的研究结果表明,脂肪组织可能不是贪食症患者TNF-α的直接来源,但这些患者血浆TNF-α的升高可能源自中枢神经系统。与sTNF-RI相比,贪食症患者中升高的sTNF-RII可能反映了不同的脱落动力学。