THE ROLE OF NOVEL GUT-BONE SIGNALING IN OSTEOPOROSIS
(Conferences / Seminars / Lectures)
HOST: Anne Dorrance
It is estimated that by 2020 more than 61 million men and women will have osteoporosis. In fact, one in three women over the age of 50 will experience an osteoporosis related fracture in their lifetime. Along with its associated increase in fracture risk, bone loss may have negative effects on metabolism and insulin secretion. Despite all the anti-resorptive treatments on the market, the number of osteoporotic patients is on the rise in the U.S. and worldwide. Bone loss can be caused by a variety of factors including aging, menopause, and diseases such as those examined in my laboratory: type 1 diabetes and inflammatory bowel disease. Diagnosis of T1D is increasing in children and adults. While medical advances are extending patient lifespan, maintaining euglycemia remains difficult, even under therapeutic vigilance. Thus, more T1D patients are suffering from complications, including bone loss and its associated increased fracture risk. We demonstrate that T1D suppresses bone formation and strength while altering bone marrow cell populations and increasing marrow adiposity. We have incorporated co-culture models, genetically modified mouse models and human studies to identify potential mechanisms/therapeutic targets. Similarly, we have used the same approaches to examine mechanisms of inflammatory bowel disease, which led us to identify the gut as a potential mediator of bone loss. We are now focusing on the role of the gut environment as a signal regulating bone loss in type 1 diabetes as well as in estrogen deficiency (as is associated with menopause). We have identified significant gut changes that relate to bone health. Taken together, our studies are moving toward identifying basic signaling mechanisms relating the GI tract to bone health.