× Home Personnel Research Publications Blog Brain Freeze Contact Us

RESEARCH

Neurobiology of Obesity


Obesity is a worldwide epidemic. It is multifactorial and yields significant medical consequences, including diabetes, cardiovascular disease, liver disease, and even cancer. Few therapies have emerged to treat obesity, but this is not surprising because we cannot fix a problem that we do not fully understand.

The brain is a vital organ that controls how much we eat and how many calories we burn. However, eating is a very complex behaviour. We eat when we are hungry, but do not eat only when we are hungry, and there lies the problem. In the Chee lab, we tackle this problem by studying the homeostatic factors that control hunger; the hedonic factors that stimulate or curb appetite; as well as how food nutrition delivers brain signals to promote healthy or unhealthy behaviors.


Click on the cards to learn more.



HOMEOSTATIC

In order to understand how the brain coordinates feeding behavior, it is necessary to identify the key players and brain regions involved. The key players acting in the brain to regulate hunger may be neuropeptides or hormones made within the brain, or they may be made in the peripheral organs (e.g. pancreas, gut, liver, etc). We are particularly interested in the roles of melanin-concentrating hormone (MCH), which is made exclusively with the brain; ghrelin, a gut peptide; and fibroblast growth factor 21 (FGF21), which is primarily released by the liver, pancreas, and fat cells.
NUTRITION

We are what we eat. More than just feeding our bodies, nutrients like fats, sugars, and protein, have also have a significant impact on brain neurochemistry. We are particularly interested in the role of fructose on the neurobiology of obesity. Fructose is a simple sugar that tastes sweeter than glucose and bonds with glucose to make table sugar. We consume fructose in excess by consuming soda and juices, packaged goods, baked goods, and even dairy products that contain added sugars. It has been linked to the development of obesity and Type II diabetes thus research in our lab will test if fructose-rich diets promote neuroplasticity leading to diet-induced obesity. We compare the healthy and unhealthy brain to learn and prevent diet-mediated maladaptations that tip the body weight scale.
NUTRITION

We are what we eat. More than just feeding our bodies, nutrients like fats, sugars, and protein, have also have a significant impact on brain neurochemistry. We are particularly interested in the role of fructose on the neurobiology of obesity. Fructose is a simple sugar that tastes sweeter than glucose and bonds with glucose to make table sugar. We consume fructose in excess by consuming soda and juices, packaged goods, baked goods, and even dairy products that contain added sugars. It has been linked to the development of obesity and Type II diabetes thus research in our lab will test if fructose-rich diets promote neuroplasticity leading to diet-induced obesity. We compare the healthy and unhealthy brain to learn and prevent diet-mediated maladaptations that tip the body weight scale.










HEDONIC

Invariably, there are many factors determining when, what, and how much we eat. Our lab is investigating these underlined factors by first considering the neural circuit - the functional connections and pathways between brain regions - that control appetite and satiety.

The hypothalamus, located at the base of the brain, is a vital brain region for the control of body weight and food intake. We are evaluating hypothalamic connectivity with the forebrain, midbrain, and hindbrain to determine how brain communication signals appetite and satiety. Furthermore, we are also evaluating which chemical messengers enable this communication. To do this, we are studying the interactions between endogenous hormones and neurotransmitters by applying ex vivo electrophysiology and optogenetics to behavioral or transgenic mouse models.

PARTNERS & AFFILIATIONS