Seminar – David A. Bernlohr, Ph.D.
Event Date & TimeFebruary 22, 2023 at 12 Noon
DEPARTMENT OF PHARMACOLOGY
Wednesday, February 22, 2023
12:00pm – 444B LSOM
David A. Bernlohr, Ph.D.
Distinguished McKnight Professor and Head
Cargill Chair in Systems Biology of Human Metabolism
Department of Biochemistry, Molecular Biology, and Biophysics
University of Minnesota - Twin Cities
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About the Speaker(s)
The Bernlohr laboratory is focused on understanding the molecular alterations that arise due to obesity, from the expanded adipose tissue to its associated pathologies, including type 2 diabetes, inflammation and cancer (Bernlohr). Within that goal, projects within the lab can be grouped into three major themes:
Adipose Biology and Obesity Linked Insulin Resistance: Role of FABPs, UCP2, and Inflammation
A major research area in the laboratory focuses on the metabolic relationships between obesity and insulin action. Many studies have shown a strong connection of obesity to chronic, low-grade inflammatory state in adipose tissue. Using a combination of biochemical, biophysical and molecular methodologies, the laboratory studies adipocytes, as well as the accumulation of inflammatory macrophages and other immune cells in adipose tissue. Specifically we examine fatty acid binding proteins and their role(s) in mediating fatty acid metabolism in adipocytes and macrophages. The adipocyte fatty acid binding protein (FABP4) binds a long chain fatty acid, providing solubility and proper cellular trafficking of fatty acids. Using FABP4 null animal models, we (and others) have shown a major protection from obesity-dependent diseases. Recently, we have discovered an inverse relationship in the expression of FABP4 and uncoupling protein 2 (UCP2) in adipose macrophages, and furthermore that UCP2 underlies many of the protective affects of reduced FABP4 expression. These experiments demonstrate the importance of the metabolic flexibility in macrophages, ie altered fatty acid fates, as contributors to health and disease. Such studies provide a framework for the analysis of obesity-linked insulin resistance.