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Laurie J. Goodyear, Ph.D.

Dr. Goodyear is a Senior Investigator and Head of the Section on Integrative Physiology and Metabolism at Joslin, and an Associate Professor of Medicine at Harvard Medical School. She received her Ph.D. in Cell Biology from the University of Vermont, and postdoctoral training included fellowships at Vermont, Harvard Medical School and in the Section on Metabolism at Joslin.  

Dr. Goodyear is an active member of the American Diabetes Association (ADA), American Physiological Society and the American College of Sports Medicine. She has served as a member of the National Institutes of Health Study Sections on Respiratory and Applied Physiology and on Skeletal Muscle Biology. Dr. Goodyear’s awards and honors include the Mary K. Iacocca Fellowship from Joslin, a New Investigator Award from the American College of Sports Medicine, and Career Development Awards from the ADA and Juvenile Diabetes Research Foundation.

The 1996 report of the U.S. Surgeon General states that regular physical exercise results in numerous health benefits including a reduced risk of developing type 2 diabetes. Physical exercise is also widely accepted as an effective method of decreasing blood glucose concentrations in patients with diabetes. Despite the profound clinical importance of the metabolic effects of exercise, until recently there was little focus on understanding the underlying molecular mechanisms that mediate glucose transport and insulin sensitivity. A major goal of the laboratory of Dr. Goodyear is to elucidate these mechanisms.

In one area of research, Dr. Goodyear is studying how exercise signals the contracting skeletal muscles to take up glucose—a mechanism she has shown to be different from the mechanisms through which insulin signals muscle cells to take up glucose. Dr. Goodyear is now searching for clues to describe the exercise effect, including how the energy status of the muscle changes during exercise and how these changes might signal proteins which activate glucose transporter molecules in the cell to move to the cell surface and take up glucose. She has found that in type 2 diabetes, even if the insulin signals are not communicating with the cell—as in insulin resistance—the exercise signal works perfectly.

This research points to diet and especially exercise as the first lines of defense for type 2 diabetes. Even patients with type 1 diabetes can lower their insulin requirements with exercise. In particular, Dr. Goodyear identified a number of different proteins that may be involved in exercise-activated glucose uptake. For example, her research provided strong evidence that the molecule AMP kinase is part of the signaling mechanism by which exercise increases glucose transport in skeletal muscle, and she is searching for additional proteins that function in similar ways.

A second line of research focuses on MAP kinase proteins, which are activated strongly by exercise and which have different functions from the AMP kinase proteins. Instead of controlling glucose transport, the MAP kinase proteins control gene transcription, synthesizing new proteins that change the long-term adaptation of the muscle, improving its metabolic function and its structure: The muscle burns fuel (fat) more efficiently and becomes stronger.

Dr. Goodyear is also working to decipher the functions of the proteins Akt and GSK3, which work with insulin and are implicated in the regulation of glycogen metabolism in muscle. These proteins may increase post-exercise insulin sensitivity in muscle cells.

Looking ahead, Dr. Goodyear’s laboratory will be developing novel models to understand the molecular mechanisms resulting from regular exercise that prevent or attenuate not only glucose levels, but also heart disease, hypertension, lipid disorders and various forms of cancer.

Selected References
Yu H, Hirshman MF, Fujii N, Pomerleau JM, Peter LE, Goodyear LJ.  Muscle-specific overexpression of wild type and R225Q mutant AMP-activated protein kinase  #3 subunit differentially regulates glycogen accumulation.  Am J Physiol Endocrinol Metab 2006, in press

Kramer HF, Witczak CA, Fujii N, Hirshman MF, Jessen N, Taylor EB, Arnolds D, Sakamoto K, Goodyear LJ.  Distinct signals regulate AS160 phosphorylation in response to insulin, AICAR, and contraction in mouse skeletal muscle. Diabetes 2006, in press

Fujii N, Hirshman MF, Kane EM, Ho RC, Peter LE, Seifert MM, Goodyear LJ.  AMP-activated protein kinase a2 activity is not essential for contraction- and hyperosmolarity-induced glucose transport in skeletal muscle. J Biol Chem 280:39033-39041, 2005.

Ho RC, Alcazar O, Fujii N, Hirshman MF, Goodyear LJ. p38#  MAPK regulation of glucose transporter expression and glucose uptake in L6 myotubes and mouse skeletal muscle. Am J Physiol Regul Integr Comp Physiol 286:R342-R349, 2004.

Musi N, Hirshman MF, Nygren J, Svanfeldt M, Bavenholm P, Rooyackers O, Zhou G, Williamson JM, Ljunqvist O, Efendic S, Moller DE, Thorell A, Goodyear LJ. Metformin increases AMP-activated protein kinase activity in skeletal muscle of subjects with type 2 diabetes. Diabetes 51:2074-2081, 2002.

Wojtaszewski JFP, Higaki Y, Hirshman MF, Michael MD, Dufresne SD, Kahn CR, Goodyear LJ. Exercise modulates postreceptor insulin signaling and glucose transport in muscle-specific insulin receptor knockout mice. J Clin Invest 104:1257-1264, 1999.

Page last updated: April 23, 2014