Our research group studies the molecular pathways that regulate glucose and energy balance in the body. These are critical areas of study related to the worldwide epidemic of obesity and diabetes. Specifically, we focus on the cell cycle – the process of cell division and replication that contributes to tissue development and renewal. We also study the growth factors involved in cellular signaling. Our group uses mouse models to study these processes. Specifically, we focus on signaling molecules, insulin-releasing beta cells, glucose regulation, and energy homeostasis.
Signaling molecules regulate the basic activity within cells. Transforming growth factor beta (TGF-beta) is a large family of signaling molecules. Research suggests that TGF-beta influence pancreatic development and diseases. TGF-beta levels are elevated in diabetes and obesity. Using various methods, we study how this family of signaling molecules influences these diseases.
Our research demonstrated that TGF-beta triggers a signal that represses the ability of insulin to regulate the expression of specific genes. In our studies, we found that blocking this signal protects mice from obesity and diabetes. It also protected mice from developing the fatty liver that often accompany these conditions. Our findings suggest that modulating TGF-beta might treat these conditions.
Insulin-releasing beta cells
The cell cycle involves an enzyme called Cdk4. Our research shows that this enzyme regulates beta cell mass. The beta cell’s sensitivity to Cdk4 suggests potential diabetes therapies. Our group is investigating the molecular pathways that increase beta cell mass.
Glucose regulation and energy homeostasis
Glucose is the main sugar that passes through the gut and into the bloodstream. When an individual has blood glucose (blood sugar) levels that are above the normal range, they are at risk for or have diabetes. Homeostasis is the ability to maintain a constant internal environment in response to environmental changes.
We study how cell cycle regulators influence both glucose tolerance and homeostasis. We compare cell cycle molecules and biological pathways in obesity and diabetes. To do this, we use mouse models with Cdk mutations. Initial findings suggest that Cdks help modulate energy balance. We are testing whether Cdk regulates fat and muscle.