【摘要】 目的:探讨伴药源性肥胖精神分裂症患者事件相关电位P300特征、血清脑源性神经营养因子(BDNF)水平及胰岛素抵抗的状况。方法:对伴药源性肥胖的精神分裂症患者32例(肥胖组)、不伴药源性肥胖的精神分裂症患者47例(非肥胖组)及正常人42名(正常组)。以事件相关电位P300评价其认知功能,酶免疫法测定血清BDNF水平,常规检测血脂及胰岛素抵抗指数(HOMA-IR)。结果:肥胖组P300潜伏期较非肥胖组和正常组延长(P均<0. 01),非肥胖组P300潜伏期也较正常组延长(P <0. 01);肥胖组P300波幅较非肥胖组和正常组下降(P均<0. 01),非肥胖组P300波幅也较正常组下降(P <0. 01);肥胖组、非肥胖组及正常组之间血清BDNF水平差异无统计学意义(F=1. 81,P>0. 05);肥胖组HOMA-IR高于非肥胖组及正常组(均P <0. 01);精神分裂症患者中P300潜伏期与HOMA-IR呈正相关(r=0. 34,P <0. 01),P300波幅与HOMA-IR呈负相关(r=-0. 29,P <0. 05)。结论:伴药源性肥胖的精神分裂症有更明显的认知功能缺陷,并与BDNF无关;胰岛素抵抗可能参与了药源性肥胖相关认知损害的病理生理过程。更多还原

【Abstract】 Objective: To explore the characteristics of event related potential P300,the change of serum level of brain-derived neurotrophic factor(BDNF) and the status of insulin resistance in schizophrenics with obesity induced by antipsychotics. Method: 32 schizophrenics with obesity induced by antipsychotics(obesity group),47 schizophrenics without obesity induced by antipsychotics(non-obesity group) and 42 normal subjects(normal group) were enrolled. Cognitive function in all subjects was evaluated with event related potential P300. Serum level of BDNF in all subjects was measured by enzyme immunoassays. Blood lipids and homeostasis model assessment of insulin resistance(HOMA-IR) in all subjects were routinely detected. Results: P300 latency in obesity group was longer than that in non-obesity group and normal group(all P < 0. 01). P300 latency in non-obesity group was also longer than that in normal group(P < 0. 01). P300 amplitude in obesity group was lower than that in non-obesity group and normal group(all P < 0. 01). P300 amplitude in non-obesity group was also lower than that in normal group(P < 0. 01). No significant difference was observed in serum level of BDNF among obesity group,non-obesity group and normal group(F = 1. 81,P > 0. 05). HOMA-IR in obesity group was higher than that in non-obesity group and normal group(all P < 0. 01). P300 latency was positively correlated with HOMA-IR in schizophrenics(r = 0. 34,P < 0. 01). P300 amplitude was negatively correlated with HOMAIR in schizophrenics(r =-0. 29,P < 0. 05). Conclusion: Schizophrenics with obesity induced by antipsychotics has more obvious cognitive deficit,which is not correlated with BDNF. Insulin resistance may be involved in the pathophysiological process of cognitive impairment associated with obesity induced by antipsychotics.更多还原