High-Salt Diet Causes Sleep Fragmentation in Young Drosophila Through Circadian Rhythm and Dopaminergic Systems

Salt (sodium chloride) is an essential dietary requirement, but excessive consumption has long-term adverse consequences. A high-salt diet (HSD) increases the risk of chronic diseases such as cardiovascular conditions and diabetes and is also associated with poor sleep quality. Little is known, howe...

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Bibliographic Details
Published in:Frontiers in neuroscience 2019-11, Vol.13, p.1271-1271
Main Authors: Xie, Jiayu, Wang, Danfeng, Ling, Shengan, Yang, Guang, Yang, Yufeng, Chen, Wenfeng
Format: Article
Language:English
Subjects:
Aging
Behavior
Chloride
Chronic illnesses
Circadian rhythm
Circadian rhythms
Diabetes mellitus
Diet
Disease
Dopamine
Dopamine receptors
dopaminergic system
Drosophila
Food
Gene expression
high-salt diet
Homeostasis
Insects
Mammals
Metabolism
Nervous system
Neuroscience
Phenotypes
Physiology
Salt
Sleep
Sodium chloride
Studies
Sucrose
Survival analysis
Syrups & sweeteners
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Summary:Salt (sodium chloride) is an essential dietary requirement, but excessive consumption has long-term adverse consequences. A high-salt diet (HSD) increases the risk of chronic diseases such as cardiovascular conditions and diabetes and is also associated with poor sleep quality. Little is known, however, about the neural circuit mechanisms that mediate HSD-induced sleep changes. In this study, we sought to identify the effects of HSD on the sleep and related neural circuit mechanisms of . Strikingly, we found that HSD causes young to exhibit a fragmented sleep phenotype similar to that of normal aging individuals. Importantly, we further showed that HSD slightly impairs circadian rhythms and that the HSD-induced sleep changes are dependent on the circadian rhythm system. In addition, we demonstrated that HSD-induced sleep changes are dopaminergic-system dependent. Together, these results provide insight into how elevated salt in the diet can affect sleep quality.
ISSN:1662-4548
1662-453X
1662-453X
DOI:10.3389/fnins.2019.01271