首页    期刊浏览 2024年12月04日 星期三
登录注册

文章基本信息

  • 标题:Chronic treatment with dexamethasone alters clock gene expression and melatonin synthesis in rat pineal gland at night
  • 作者:Daniela Meneses-Santos ; Daniella do Carmo Buonfiglio ; Rodrigo Antonio Peliciari-Garcia
  • 期刊名称:Nature and Science of Sleep
  • 印刷版ISSN:1179-1608
  • 电子版ISSN:1179-1608
  • 出版年度:2018
  • 卷号:10
  • 页码:203-215
  • DOI:10.2147/NSS.S158602
  • 语种:English
  • 出版社:Dove Medical Press Ltd
  • 摘要:Background: Melatonin is a neuroendocrine hormone that regulates many functions involving energy metabolism and behavior in mammals throughout the light/dark cycle. It is considered an output signal of the central circadian clock, located in the suprachiasmatic nucleus of the hypothalamus. Melatonin synthesis can be influenced by other hormones, such as insulin and glucocorticoids in pathological conditions or during stress. Furthermore, glucocorticoids appear to modulate circadian clock genes in peripheral tissues and are associated with the onset of metabolic diseases. In the pineal gland, the modulation of melatonin synthesis by clock genes has already been demonstrated. However, few studies have shown the effects of glucocorticoids on clock genes expression in the pineal gland. Results: We verified that rats treated with dexamethasone (2 mg/kg body weight, intraperitoneal) for 10 consecutive days, showed hyperglycemia and pronounced hyperinsulinemia during the dark phase. Insulin sensitivity, glucose tolerance, melatonin synthesis, and enzymatic activity of arylalkylamine N -acetyltransferase, the key enzyme of melatonin synthesis, were reduced. Furthermore, we observed an increase in the expression of Bmal1 , Per1 , Per2 , Cry1 , and Cry2 in pineal glands of rats treated with dexamethasone. Conclusion: These results show that chronic treatment with dexamethasone can modulate both melatonin synthesis and circadian clock expression during the dark phase.
  • 关键词:clock genes; glucocorticoids; pineal gland; nocturnal insulinemia; glycemia profile; AANAT activity
Loading...
联系我们|关于我们|网站声明
国家哲学社会科学文献中心版权所有