The Antidepressants and the Metabolic Syndrome

Kolcsár Melinda, Gáll Zsolt, Bába László-István, K. Zoltán
{"title":"The Antidepressants and the Metabolic Syndrome","authors":"Kolcsár Melinda, Gáll Zsolt, Bába László-István, K. Zoltán","doi":"10.2478/orvtudert-2018-0009","DOIUrl":null,"url":null,"abstract":"Abstract The relationship between antidepressants (AD) and metabolic syndrome (MS) can be approached from many perspectives. We can start from the mutuality of depression and MS: depression often causes MS and vice versa; however, the two diseases aggravate each other. Altered glucocorticoid secretion - among others - may be a common etiological factor for depression and MS. Enhanced glucocorticoid production leads both to sleep disorders and insulin resistance, and several antidepressants cause obesity and insulin resistance. In addition, sympathetic nervous system activity increases in depression, together with the elevated production of counter-insulin hormones such as catecholamines (adrenaline) and glucocorticoids. From the components of MS, body weight changes can be most easily followed by the patient. The obesogenic mechanisms of AD drugs are different. The H1-receptor blocking agents have the most important weight gaining effect, followed by the 5-HT2c-receptor blocking and/or down-regulating ADs. The fattening effect of mirtazapine, paroxetine, and tricyclic antidepressants are based on such central mechanisms. Blocking of alpha1-receptors contributes to the obesogenic effects of certain drugs by inducing sedation: this has been confirmed in case of imipramine, amitriptyline, and doxepin. Fluoxetine behaves differently depending on the dose and duration of treatment: while at the usual doses it induces weight loss at the beginning of therapy, its initial anorexigenic effects reverses during prolonged use; while its activation effect at high doses is favorable in bulimia. The selective noradrenaline reuptake inhibitor reboxetine reduces appetite, similarly to bupropion, which inhibits dopamine reuptake as well. We highlight the effect of fluoxetine on direct adipogenicity, mentioning its preadipocyte-adipocyte transformation-reducing and adipocyte proliferation-inhibiting activity, as well as its ability to enhance fat cell autophagy.","PeriodicalId":9334,"journal":{"name":"Bulletin of Medical Sciences","volume":"27 1","pages":"89 - 98"},"PeriodicalIF":0.0000,"publicationDate":"2018-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Bulletin of Medical Sciences","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2478/orvtudert-2018-0009","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Abstract The relationship between antidepressants (AD) and metabolic syndrome (MS) can be approached from many perspectives. We can start from the mutuality of depression and MS: depression often causes MS and vice versa; however, the two diseases aggravate each other. Altered glucocorticoid secretion - among others - may be a common etiological factor for depression and MS. Enhanced glucocorticoid production leads both to sleep disorders and insulin resistance, and several antidepressants cause obesity and insulin resistance. In addition, sympathetic nervous system activity increases in depression, together with the elevated production of counter-insulin hormones such as catecholamines (adrenaline) and glucocorticoids. From the components of MS, body weight changes can be most easily followed by the patient. The obesogenic mechanisms of AD drugs are different. The H1-receptor blocking agents have the most important weight gaining effect, followed by the 5-HT2c-receptor blocking and/or down-regulating ADs. The fattening effect of mirtazapine, paroxetine, and tricyclic antidepressants are based on such central mechanisms. Blocking of alpha1-receptors contributes to the obesogenic effects of certain drugs by inducing sedation: this has been confirmed in case of imipramine, amitriptyline, and doxepin. Fluoxetine behaves differently depending on the dose and duration of treatment: while at the usual doses it induces weight loss at the beginning of therapy, its initial anorexigenic effects reverses during prolonged use; while its activation effect at high doses is favorable in bulimia. The selective noradrenaline reuptake inhibitor reboxetine reduces appetite, similarly to bupropion, which inhibits dopamine reuptake as well. We highlight the effect of fluoxetine on direct adipogenicity, mentioning its preadipocyte-adipocyte transformation-reducing and adipocyte proliferation-inhibiting activity, as well as its ability to enhance fat cell autophagy.
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
抗抑郁药和代谢综合征
抗抑郁药(AD)与代谢综合征(MS)的关系可以从多个角度探讨。我们可以从抑郁症和多发性硬化症的相互关系入手:抑郁症往往导致多发性硬化症,反之亦然;然而,这两种疾病相互加剧。糖皮质激素分泌的改变可能是抑郁症和多发性硬化症的常见病因之一。糖皮质激素分泌的增加会导致睡眠障碍和胰岛素抵抗,而一些抗抑郁药物会导致肥胖和胰岛素抵抗。此外,抑郁症患者交感神经系统活动增加,同时抗胰岛素激素如儿茶酚胺(肾上腺素)和糖皮质激素的分泌增加。从MS的组成来看,体重的变化最容易被患者跟踪。AD药物致肥机制不同。h1受体阻滞剂具有最重要的增重作用,其次是5- ht2c受体阻滞剂和/或下调ad。米氮平、帕罗西汀和三环抗抑郁药的增肥作用就是基于这样的中心机制。α - 1受体的阻断通过诱导镇静有助于某些药物的致肥作用:这已在丙咪嗪、阿米替林和多塞平的情况下得到证实。氟西汀的作用因剂量和治疗持续时间的不同而不同:在常规剂量下,氟西汀在治疗开始时引起体重减轻,但在长期使用期间,其最初的厌氧作用会逆转;而在高剂量时,其活化作用对暴食症有利。选择性去甲肾上腺素再摄取抑制剂瑞波西汀可以减少食欲,类似于抑制多巴胺再摄取的安非他酮。我们强调了氟西汀对直接脂肪生成的影响,提到了它的前脂肪细胞-脂肪细胞转化减少和脂肪细胞增殖抑制活性,以及它增强脂肪细胞自噬的能力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
Quality by design-based method development for the determination of related substances of ezetimibe by high performance liquid chromatography Determination of the sun protection factor of sunscreens Alzheimer’s disease beyond the amyloid accumulation Radioactive background radiation measurement in Mureş county Study of pulmonary complications in patients referred to the intensive care unit
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1