Role for intestine-bone signaling pathways in regulating osteoporosis PDF
Laura R. McCabe, Department of Physiology, Michigan State University

1/14/2013, 2pm, GHC 9115


Osteoporosis, significant bone loss and fragility, affects more than 10 million people in the US. Fifty percent of women and 25% of men will have an osteoporotic-related fracture in their lifetime. Understanding mechanisms regulating bone density is critical given the increased mortality, dependency and morbidity associated with a bone break in the elderly. My lab is focused on identifying mechanisms of disease induced bone loss. We, along with others, show that inflammatory bowel disease decreases bone density and growth in a mouse model. We further identify that even low levels of intestinal inflammation can lead to bone loss. In addition, diseases like type 1 diabetes that cause bone loss are also associated with intestinal changes. We hypothesize that signals move between the gut and bone (and possibly liver) to modify bone density under healthy versus diseased conditions. Possible regulatory pathways include vitamin D metabolism, lipid metabolism and wnt signaling. We are working in cell culture, mouse models and humans. A variety of approaches are used to assess disease-induced changes in cell/organ function, growth, inflammation and signaling pathways. Our goal is to identify novel intestinal-bone regulatory pathways and therapeutic targets.


Laura McCabe is a Professor of Physiology and Radiology and is currently Associate Chair of Physiology.  She received her undergraduate degree in Biology in 1986 from the University of Chicago. In graduate school at University of Chicago, she focused on intestinal physiology and disease induced changes in epithelial cell maturation and gene expression.  In 1991, she became a post-doctoral student in the Department of Cell Biology at University of Massachusetts Medical Center, where she examined the molecular regulation of bone cell function. In 1996 she joined the faculty at Michigan State University.  Her current research focuses on understanding mechanisms regulating bone cell differentiation and bone formation. The laboratory incorporates several models of induced bone loss including: type 1 diabetes, inflammatory bowel disease and menopause. Identifying the novel roles of inflammation and altered signaling in these models that leads to bone loss will be critical in the ultimate identification of therapeutic treatment targets.


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nsfSupported by an Expeditions in Computing award from the National Science Foundation