At the Bergman Laboratory in the Cedars-Sinai Diabetes and Obesity Research Institute, we are studying the relationships between obesity, insulin resistance, and diabetes. We are examining the mechanisms by which increased stored fat reduces the sensitivity of tissues, especially skeletal muscle and fat, to the hormone insulin. We are studying why resistance to the hormone insulin predisposes individuals to diabetes mellitus, defined as increased blood glucose. Our goal is to identify compounds or procedures that can reduce obesity or that can suppress the linkage between obesity and insulin resistance, and between insulin resistance and Type 2 diabetes. We are studying the mechanisms underlying beta-cell failure, and how failure of the pancreatic beta cells interacts with insulin resistance to cause diabetes. We are examining therapies for diabetes, including implanted devices to treat the disease, as well as stem-cell (regenerative medicine) approaches to compensate for reduced beta-cell function. We are studying the importance of the gut-brain axis in glucose regulation, particularly with regard to the gut hormone GLP-1 and how signals in the abdominal portal vein are detected by specific sensors, and the role of said sensors in carbohydrate metabolism.
The Bergman Laboratory is affiliated with the Diabetes & Obesity Research Institute and the Department of Biomedical Sciences.
I was originally trained as an electrical engineer at Case Institute of Technology (now Case-Western Reserve University). This training led to my appreciation of how systems composed of different components can work together to achieve a common goal. I believed that this "systems approach" had wider applicability."
Richard Bergman, PhD
We have discovered that free fatty acids, common lipid molecules in blood, change with time. We reported in animals that FFAs are elevated in the middle of the night (3 am), a result that has been replicated in human volunteers. We have hypothesized that this nocturnal surge in FFA has important metabolic consequences: that is, not only does it contribute to glucose intolerance, but the surge is also responsible for the increase in insulin secretory function that normally accompanies insulin resistance. It is the failure of the pancreatic islets (i.e., beta-cells) to compensate for insulin resistance that is responsible for the prediabetic state. We are examining the explicit role of the FFA surge in the pathogenesis of Type 2 diabetes.
Collaborations & Resources
- Biomedical Imaging Research Institute
- Division of Endocrinology, Diabetes and Metabolism
- Division of Gastroenterology
- Department of Obstetrics and Gynecology
- Department of Surgery
- Smidt Heart Institute
- Medical Genetics Institute
Meet Our Team
Learn more about the scientists, faculty members, investigators and other healthcare professionals of the Bergman Laboratory, whose dedicated efforts lead to groundbreaking discoveries.
Kolka CM, Castro AV, Kirkman EL, Bergman RN.
Metabolism. 2015 Feb;64(2):330-337.
Ionut V, Castro AV, Woolcott OO, Stefanovski D, Iyer MS, Broussard JL, Burch M, Elazary R, Kolka CM, Mkrtchyan H, Bediako IA, Bergman RN.
Am J Physiol Endocrinol Metab. 2014 Oct 15;307(8):E644-652.
Woolcott OO, Castillo OA, Gutierrez C, Elashoff RM, Stefanovski D, Bergman RN.
Obesity (Silver Spring). 2014 Sep;22(9):2080-2090.
Contact the Bergman Lab
8730 Alden Drive.
Thalians Building, Room E104
Los Angeles, CA 90048