Animals are keenly tuned to adapt their behavior in response to environmental changes. The absence of food represents a common environmental challenge that requires behavioral and metabolic adaptation. Animals respond to starvation by suppressing sleep in order to forage for food. This starvation-induced sleep suppression involves communication between endocrine systems that relay nutrient availability between adipose tissue and the brain. The fruit fly, Drosophila melanogaster, like mammals, suppresses sleep in order to forage for food and utilizes many conserved molecular pathways including insulin and glucagon-like signaling to control homeostasis and metabolism. Due to the high conservation of metabolic systems and behavior between flies and mammals, the experiments outlined here will provide biological information applicable beyond the fruit fly to elucidate the general mechanisms through which metabolism regulates behavior. Preliminary data from the PIs indicates a role for the Drosophila insulin and the glucagon-like hormone (AKH) pathways in controlling sleep when food is limited. These findings led to the hypothesis that insulin and AKH signal changes in nutrient levels to induce the animal to alter its behavior accordingly. To address this hypothesis, the metabolic substrate(s) required for normal sleep will be identified through dietary and pharmacological manipulation of nutrient stores. Additionally, this proposal seeks to determine the mechanisms whereby insulin and AKH signaling control hunger-induced sleep suppression and whether this occurs through long-term changes in nutrient stores or acute regulation of fat body function. Taken together, this research plan employs behavioral and metabolic analysis to examine how distinct tissue types sense hunger and communicate to initiate adaptive behavior. These experiments wil further our understanding of how metabolism regulates behavior and provide insight into the underlying basis of metabolism-linked disorders.

Public Health Relevance

Dysregulation of both sleep and feeding behaviors presents an enormous health burden throughout the world, and interactions between these two behaviors have many clinical manifestations that include obesity in short- sleeping individuals and sleep disturbances in the undernourished. The metabolic substrate(s) required for normal sleep will be identified through dietary and pharmacological manipulation of nutrient stores. Additionally, this proposal seeks to determine the mechanisms whereby insulin and AKH signaling control hunger-induced sleep suppression and whether this occurs through long-term changes in nutrient stores or acute regulation of fat body function.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Academic Research Enhancement Awards (AREA) (R15)
Project #
1R15NS080155-01A1
Application #
8491500
Study Section
Special Emphasis Panel (ZRG1-EMNR-S (90))
Program Officer
He, Janet
Project Start
2013-05-01
Project End
2016-04-30
Budget Start
2013-05-01
Budget End
2016-04-30
Support Year
1
Fiscal Year
2013
Total Cost
$368,404
Indirect Cost
$70,180
Name
University of Nevada Reno
Department
Biology
Type
Schools of Arts and Sciences
DUNS #
146515460
City
Reno
State
NV
Country
United States
Zip Code
89557
Masek, Pavel; Reynolds, Lauren A; Bollinger, Wesley L et al. (2014) Altered regulation of sleep and feeding contributes to starvation resistance in Drosophila melanogaster. J Exp Biol 217:3122-32
Robertson, Meagan; Keene, Alex C (2013) Molecular mechanisms of age-related sleep loss in the fruit fly - a mini-review. Gerontology 59:334-9
Masek, Pavel; Keene, Alex C (2013) Drosophila fatty acid taste signals through the PLC pathway in sugar-sensing neurons. PLoS Genet 9:e1003710