Research:

The long-term goal of my research is to understand the underlying molecular and cellular mechanisms regulating glucose homeostasis as they relate to type 2 diabetes and breast cancer progression.  Specifically I am investigating factors involved in the reorganization of the cytoskeleton during glucose transport.  The major defect in type 2 diabetes is insulin resistance of peripheral tissues, primarily skeletal muscle and adipose tissue. Insulin-stimulated glucose uptake requires the activation of several signaling pathways to mediate the translocation of insulin-responsive glucose transporter 4 (GLUT4) vesicles from an intracellular pool to the plasma membrane.  Identification and characterization of factors involved in glucose uptake is critical for developing more effective treatments for type 2 diabetes. My laboratory has identified myosin II, calpain 10, and naringenin as critical regulators of insulin-stimulated glucose uptake.

Scientific Publications:

Harmon, A. W. and Patel, Y. M. (2004) Naringenin inhibits glucose uptake in MCF-7 breast cancer cells: a mechanism for impaired cellular proliferation. Breast Cancer Research and Treatment 85:103-110.

Cooke, D. W. and Patel Y. M. (2005) GLUT4 expression in 3T3-L1 adipocytes is repressed by proteasome inhibition. Molecular and Cellular Endocrinology 232:37-45.

Steimle, P.A., Fulcher, K.F., Patel, Y.M. (2005) A novel role for myosin II in insulin-stimulated glucose uptake in 3T3-L1 adipocytes. Biochemical and Biophysical Research Communications. 331:1560-1565.

Turner, M. D., Fulcher, F. K., Jones, C. R., Smith, B. T., Aganna, E., Partridge, C. J., Hitman, G. A., Clark, A. and Patel, Y. M. (2007) Calpain facilitates actin reorganization during glucose-stimulated insulin secretion. Biochemical and Biophysical Research Communications 352:650-655.

Classes:

Cell Biology Laboratory (BIO 356)
Metabolic Regulation in Health and Disease (BIO 535)
Hormones in Action (BIO 578)

Contact:

207 Eberhart Building
(336) 256-0080