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Division of BioMedical Sciences


Our People - Faculty Websites - MichiruHirawasa_Ongoing-Research

Ongoing Research:

Healthy eating and good night sleep are important facets of being healthy and happy in everyday life. In modern society, however, many people struggle to fight against temptations of palatable food loaded with fat, sugar and salt, and as a result the obesity rate continues to rise. Inadequate sleep has also become increasingly common. Such disturbances in homeostasis could result in various diseases.


Our goal is to understand how the brain responds to disruption in homeostasis, such as high fat diet and sleep deprivation because the brain is responsible for detecting homeostatic challenges and countering them with autonomic and behavioral responses. Specifically, the hypothalamus regulates homeostasis, and thus investigating how neurons and glial cells (non-neuronal cells) in the hypothalamus work under normal (balanced) and unbalanced conditions will help us understand how homeostasis is maintained. 
 
Research Questions we are asking:
 
Q: How do hypothalamic neurons deal with homeostatic challenge?
Hypothesis: Homeostatic challenges usually last long-term (minutes to days). Thus neurons responsible for maintaining homeostasis may display unique forms of long-term synaptic plasticity.

Q: Why do we eat too much fatty food? 
Hypothesis: High fat diet activates appetite-inducing neurons, which in turn promote further diet intake, creating a vicious positive feedback cycle.

Q: Does repeated dieting have adverse effects on health?
Hypothesis: Repetitive dieting and weight cycling results in impaired regulation of body weight and blood glucose by the hypothalamus. 

Q: What underlies obese phenotype in Prader-Willi Syndrome?
Hypothesis: Prader-Willi Syndrome accompanies dysregulation of hypothalamic neuropeptide, which underlies obesity and other symptoms of this syndrome.

Q: How does lack of sleep affect the brain?
Hypothesis: Sleep deprivation increases sleep pressure and rebound sleep, which is due to an alteration in the way glial cells regulate neuronal activity.

 
 
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