Paul F. Pilch

photoProfessor
Associate Director, Graduate Program in Molecular Medicine

Boston University School of Medicine
Silvio Conte Building, K603
72 E. Concord Street
Boston, MA 02118

Phone: 617-638-4044
Lab Phone:
617-638-4045
Fax: 617-638-4208
Email:
ppilch@bu.edu

Joint Appointment: Department of Medicine

Education

BA, Temple University, Philadelphia, PA
PhD, Purdue University, W. Lafayette, IN

BU Profile

People

Collete LaFlamme
Student
Shiying Ding
Postdoctoral Associate
Libin Liu
Instructor
Alessandro Peschechera
Postdoctoral Associate

Research Interests

Cell biology of adipocytes and muscle

Fat cells or adipocytes play a key role in the regulation of metabolism by insulin and other hormones, and the study of this role at many levels constitutes a major activity of modern cellular and molecular biology. Adipocytes have an unusually high number of plasma membrane micro-domains called caveolae, invaginations resembling little caves, which comprise 50% of their cell surface. We have engineered mice to lack a protein component of caveolae, cavin-1, which leads to a total loss of caveolae in in all tissues and results in profound insulin resistance, lipo- and muscular dystrophy, pathologies identical to those resulting from functional loss of caveolae in humans. We are studying this physiologically relevant mouse model of multiple pathologies to understand the functions of caveolae and their roles in cellular functions in three organs, adipose, skeletal muscle and heart, all of which are dysfunctional. The broader functions affected by caveolae in a variety of cells include motility, cell surface dynamics/mechano-transduction and membrane repair, and we study these roles of caveolae as well.Pilchresearch

Adipose tissue is a robust endocrine organ that makes and secretes hormone-like proteins called adipokines, e.g., leptin and adiponectin, which in turn have profound affects on overall metabolism and energy balance. We have identified in the adipocyte endoplasmic reticulum (E.R.), a resident protein we call adiporedoxin (see the Figure) that is most highly expressed in fat cells. In vitro, adiporedoxin loss and over expression cause decreases and increases in secretion of adiponectin, respectively, and its manipulation affects many other secreted proteins in a similar manner. We created mice null for adiporedoxin, and they have a reduced level of circulating adiponectin, a marker for insulin sensitivity, and they develop glucose intolerance/insulin resistance on a high fat diet.  Data from human adipocytes show adiporedoxin expression also correlates positively with insulin sensitivity. We are exploiting our mouse model, cultured murine and human fat cells to further understand the mechanism of adiporedoxin’s actions and its affects on metabolic regulation.

Research Themes

Metabolism, Obesity/Diabetes

Representative Publications:

PubMed