期刊
AGEING RESEARCH REVIEWS
卷 20, 期 -, 页码 63-73出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.arr.2014.11.001
关键词
Orexin; Hypocretin; Obesity; Sleep; Aging; Energy balance
资金
- Department of Veterans Affairs [F7212W, 5101RX000441-04, 1IK2BX001686-01A1]
- National Institutes of Health-NIDDK [1R01DK100281-01A1]
- United States Department of Agriculture [ARZT-1360220-H23-150, ARZT-1372540-R23-131]
- VA [550452, 1IK2BX001686-01A1] Funding Source: Federal RePORTER
The hypothalamic neuropeptides orexin A and B (hypocretin 1 and 2) are important homeostatic mediators of central control of energy metabolism and maintenance of sleep/wake states. Dysregulation or loss of orexin signaling has been linked to narcolepsy, obesity, and age-related disorders. In this review, we present an overview of our current understanding of orexin function, focusing on sleep disorders, energy balance, and aging, in both rodents and humans. We first discuss animal models used in studies of obesity and sleep, including loss of function using transgenic or viral-mediated approaches, gain of function models using exogenous delivery of orexin receptor agonist, and naturally-occurring models in which orexin responsiveness varies by individual. We next explore rodent models of orexin in aging, presenting evidence that orexin loss contributes to age-related changes in sleep and energy balance. In the next section, we focus on clinical importance of orexin in human obesity, sleep, and aging. We include discussion of orexin loss in narcolepsy and potential importance of orexin in insomnia, correlations between animal and human studies of age-related decline, and evidence for orexin involvement in age-related changes in cognitive performance. Finally, we present a summary of recent studies of orexin in neurodegenerative disease. We conclude that orexin acts as an integrative homeostatic signal influencing numerous brain regions, and that this pivotal role results in potential dysregulation of multiple physiological processes when orexin signaling is disrupted or lost. Published by Elsevier B.V.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据