Excessive insulin secretion in Japanese schizophrenic patients treated with antipsychotics despite normal fasting glucose levels.
Excessive insulin secretion in Japanese schizophrenic patients treated with antipsychotics despite normal fasting glucose levels.
复制标题
尽管空腹血糖水平正常，但接受抗精神病药物治疗的日本精神分裂症患者胰岛素分泌过多。
DOI：
10.1097/jcp.0b013e3182742ea4
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发表时间：
2012
期刊：
影响因子：
--
通讯作者：
Someya T.
中科院分区：
文献类型：
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作者：
Sugai T;Suzuki Y;Fukui N;Watanabe J;Ono S;Tsuneyama N;Someya T.
抗精神病药(APs)所致的糖耐量减退是精神科药物治疗的严重副作用，引起人们的关注。然而，AP导致血糖-胰岛素反应障碍的机制尚不完全清楚。最近的研究表明，与健康对照组相比，接受AP治疗的精神分裂症患者在葡萄糖负荷后更有可能出现糖耐量受损，即使空腹血糖水平在参考范围内。为了解释这些发现，我们假设接受AP治疗的精神分裂症患者的胰岛素分泌增加，即使是那些正常的空腹血糖(NFG)水平。因此，我们对159名接受AP治疗的日本住院精神分裂症患者和90名健康的非精神分裂症患者进行了口服葡萄糖耐量试验。分别于服糖前(0分钟)、服糖后30分钟、60分钟、90分钟和120分钟测定血糖和血清胰岛素浓度。虽然两组受试者在0分钟的胰岛素水平相似，但在糖负荷后的所有时间，AP治疗的患者的胰岛素水平均显著高于健康受试者。在对NFG受试者的分析中，在糖负荷后的所有时间，AP治疗的患者的胰岛素水平都显著高于健康受试者。总体而言，我们发现，无论NFG如何，接受AP治疗的患者对糖负荷的反应所产生的胰岛素分泌显著增加。这些结果表明，AP影响葡萄糖-胰岛素反应，这可能导致在显性糖耐量异常发生之前出现亚临床胰岛素抵抗。
The development of impaired glucose tolerance induced by antipsychotics (APs) is of concern as a serious adverse effect of psychiatric drug therapy. However, the mechanism by which APs cause dysfunction of the glucose-insulin response is not fully understood. Recent studies have shown that patients treated with APs for schizophrenia were more likely to exhibit impaired glucose tolerance after a glucose load compared with healthy control subjects, even if fasting glucose levels were within the reference range. To explain these findings, we hypothesized that insulin secretion is increased in schizophrenic patients treated with AP, even those normal fasting glucose (NFG) levels. Therefore, oral glucose tolerance tests were conducted in 159 Japanese inpatients with AP-treated schizophrenia and in 90 healthy subjects without schizophrenia. Plasma glucose and serum insulin concentrations were measured before (0 minute) and at 30, 60, 90, and 120 minutes after the oral glucose load. Although insulin levels at 0 minute were similar in both groups of subjects, insulin levels were significantly higher in the patients treated with AP at all times after the glucose load than in the healthy subjects. In analyses of NFG subjects, insulin levels were significantly higher in the patients treated with AP compared with the healthy subjects at all times after glucose loading. Overall, we found that insulin secretion in response to a glucose load was significantly higher in the patients treated with AP, irrespective of NFG. These results suggest that APs affect the glucose-insulin response, which may lead to subclinical insulin resistance before the onset of overt glucose intolerance.