Elevated S100B levels in schizophrenia are associated with insulin resistance
Elevated S100B levels in schizophrenia are associated with insulin resistance
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精神分裂症患者 S100B 水平升高与胰岛素抵抗相关
DOI：
10.1038/mp.2009.87
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发表时间：
2010
影响因子：
11
通讯作者：
Bogerts B.
中科院分区：
文献类型：
--
作者：
Steiner J;Walter M;Guest P;Myint AM;Schiltz K;Panteli B;Brauner M;Bernstein H;Herberth M;Schroeter ML;Schwarz MJ;Westphal S;Bahn S;Bogerts B.
一些研究表明，精神分裂症患者的循环S100 B蛋白水平升高。1这一发现被明确归因于神经胶质病理学，因为S100 B是由星形胶质细胞和少突胶质细胞产生的，被认为是一种神经营养因子，对突触发生、多巴胺能和多巴胺能神经递质传递有影响。2然而，这项研究表明，超重和胰岛素抵抗可能是交替负责。脂肪组织已经被其他人强调为S100 B的重要脑外来源，因为它含有大量的S100 B。3，4脂肪细胞分泌的S100 B被胰岛素减少，并被生理因素如应激和禁食激活。5，6因此，考虑到精神分裂症患者及其一级亲属中代谢综合征的患病率增加，体重增加或脂肪细胞功能障碍，包括胰岛素不敏感性，可以为S100 B水平升高提供重要的替代解释。[7]脑脊液和死后脑组织中S100 B水平升高的发现对精神分裂症中S100 B水平改变的脑外起源的假设提出了挑战。8，9然而，早期的细胞培养研究表明，S100 B释放的神经胶质异常也可能是由能量供应中断引起的。[2]因此，在精神分裂症患者的背外侧前额叶皮层中观察到胰岛素信号受损。因此，外周和大脑葡萄糖使用的改变是需要研究的重要因素，以阐明其与精神分裂症中S100 B的关系。因此，我们的研究评估了服用药物和不服用药物的精神分裂症患者的S100 B，沿着体重指数（BMI）、葡萄糖使用量和脂肪因子水平。在获得书面知情同意书后，从26名急性偏执型精神分裂症患者中采集血清样本（根据DSM-IV，17名男性/9名女性，年龄34.7±11.3岁，BMI 27.7±5.7，16名吸烟者/10名不吸烟者）和32名匹配的对照（20名男性/12名女性，年龄34.4±10.8，BMI 24.3±3.8，14名吸烟者/18名不吸烟者）。11例患者未用药X6周; 15例患者接受非典型抗精神病药物治疗26±21天。采用阳性和阴性症状量表监测精神病理学。排除标准包括免疫疾病、免疫调节治疗、癌症、慢性终末期疾病、心血管疾病、糖尿病、药物滥用和严重的
Several studies have shown that circulating S100B protein levels are elevated in schizophrenia. 1 This finding has been specifically attributed to glial pathology, as S100B is produced by astro-and oligodendroglial cells and is thought to act as a neurotrophic factor with effects on synaptogenesis, dopaminergic and glutamatergic neutrotransmission. 2 However, this study suggests that overweight and insulin resistance may be alternatively responsible. Adipose tissue has already been highlighted by others as an important extracerebral source of S100B, as it contains considerable amounts of S100B. 3, 4 S100B secretion from adipocytes is reduced by insulin and is activated by physiological factors such as stress and fasting. 5, 6 Therefore, weight gain or adipocyte dysfunction, including insulin insensitivity, could offer important alternative explanations for elevated S100B levels, given the increased prevalence of metabolic syndrome in schizophrenic patients and their firstdegree relatives. 7 The assumption of such extracerebral origins of altered S100B levels in schizophrenia is challenged by findings of elevated S100B in cerebrospinal fluid and postmortem brain tissue. 8, 9 However, glial abnormalities in S100B release may also be caused by disrupted energy supply, as suggested by earlier cell culture studies. 2 Accordingly, impaired insulin signaling has been observed in the dorsolateral prefrontal cortex of schizophrenic patients. 10 Consequently, altered peripheral and cerebral glucose usage is an important factor to be studied to clarify its relation to S100B in schizophrenia. Our study thus assessed S100B in both medicated and drug-free schizophrenic patients, along with body mass index (BMI), measures of glucose usage and adipokine levels.After obtaining written informed consent, serum samples were taken from 26 patients with acute paranoid schizophrenia (according to DSM-IV, 17 men/9 women, age 34.7±11.3 years, BMI 27.7±5.7, 16 smokers/10 nonsmokers) and from 32 matched controls (20 men/12 women, age 34.4±10.8, BMI 24.3±3.8, 14 smokers/18 nonsmokers). Eleven patients were unmedicated for X6 weeks; 15 were treated with atypical antipsychotics for 26±21 days. Psychopathology was monitored using the positive and negative syndrome scale. Exclusion criteria consisted of an earlier history of immune diseases, immunomodulating treatment, cancer, chronic terminal disease, cardiovascular disorders, diabetes, substance abuse and severe
脂肪组织中的 S-100 蛋白。
DOI：
--
发表时间：
1983
期刊：
International Journal of Biochemistry
影响因子：
--
作者：
K. Kato;F. Suzuki;T. Nakajima
通讯作者：
T. Nakajima
影响因子：
3.3
作者：
Johann Steiner;H. Bernstein;B. Bogerts;T. Gos;C. Richter-Landsberg;M. Wunderlich;G. Keilhoff
通讯作者：
Johann Steiner;H. Bernstein;B. Bogerts;T. Gos;C. Richter-Landsberg;M. Wunderlich;G. Keilhoff
代谢综合征和精神分裂症。
DOI：
--
发表时间：
2005
期刊：
The British journal of psychiatry : the journal of mental science
影响因子：
--
作者：
J. Thakore
通讯作者：
J. Thakore