PUBLICATION
Impaired Sleep, Circadian Rhythms and Neurogenesis in Diet-Induced Premature Aging
- Authors
- Stankiewicz, A.J., McGowan, E.M., Yu, L., Zhdanova, I.V.
- ID
- ZDB-PUB-171028-14
- Date
- 2017
- Source
- International Journal of Molecular Sciences 18(11): (Journal)
- Registered Authors
- Zhdanova, Irina
- Keywords
- anxiety, cell cycle, circadian, diurnal vertebrate, high caloric intake, neurogenesis, premature aging, scoliosis, sleep
- MeSH Terms
-
- Aging, Premature/etiology*
- Animals
- Anxiety
- Body Weight
- Brain/metabolism
- Brain/pathology
- Brain/physiopathology
- Circadian Clocks
- Circadian Rhythm*
- Energy Intake
- Gene Expression
- Neurogenesis*
- Organ Size
- Sleep*
- Sleep Wake Disorders/complications*
- Sleep Wake Disorders/physiopathology*
- Zebrafish
- PubMed
- 29072584 Full text @ Int. J. Mol. Sci.
Citation
Stankiewicz, A.J., McGowan, E.M., Yu, L., Zhdanova, I.V. (2017) Impaired Sleep, Circadian Rhythms and Neurogenesis in Diet-Induced Premature Aging. International Journal of Molecular Sciences. 18(11).
Abstract
Chronic high caloric intake (HCI) is a risk factor for multiple major human disorders, from diabetes to neurodegeneration. Mounting evidence suggests a significant contribution of circadian misalignment and sleep alterations to this phenomenon. An inverse temporal relationship between sleep, activity, food intake, and clock mechanisms in nocturnal and diurnal animals suggests that a search for effective therapeutic approaches can benefit from the use of diurnal animal models. Here, we show that, similar to normal aging, HCI leads to the reduction in daily amplitude of expression for core clock genes, a decline in sleep duration, an increase in scoliosis, and anxiety-like behavior. A remarkable decline in adult neurogenesis in 1-year old HCI animals, amounting to only 21% of that in age-matched Control, exceeds age-dependent decline observed in normal 3-year old zebrafish. This is associated with misalignment or reduced amplitude of daily patterns for principal cell cycle regulators, cyclins A and B, and p20, in brain tissue. Together, these data establish HCI in zebrafish as a model for metabolically induced premature aging of sleep, circadian functions, and adult neurogenesis, allowing for a high throughput approach to mechanistic studies and drug trials in a diurnal vertebrate.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping