September 28, 2009
Diabetes Weakens Your Bones
Current research suggests that the inflammatory molecule TNF-Ã± may contribute to delayed bone fracture healing in diabetics. The related report by Alblowi et al, "High Levels of TNF-Ã± Contribute to Accelerated Loss of Cartilage in Diabetic Fracture Healing" appears in the October 2009 issue of the American Journal of Pathology.
Diabetes, a condition where the body either does not produce enough, or respond to, insulin, affects at least 171 million people worldwide, a figure that is likely to double by 2030. Long-term complications of diabetes include cardiovascular disease, chronic renal failure, retinal damage that may lead to blindness, nerve damage, and blood vessel damage, which may cause erectile dysfunction and poor wound healing.
Alblowi et al suggest that "TNF-Ã± dysregulation plays a prominent role in the recently identified catabolic events associated with diabetic fracture healing." In future studies, Dr. Graves and colleagues plan to "examine the effect of FOXO1 on mineralized tissue to examine how it may regulate factors that control bone resorption and osteoclastogenesis, in addition to effects it may have on osteoblastic cells."
This work was supported by grants from the National Institutes of Health.
Alblowi J, Kayal RA, Siqueira M, McKenzie E, Krothapalli N, McLean J, Conn J, Nikolajczyk B, Einhorn TA, Gerstenfeld L, Graves DT: High Levels of TNF-Ã± Contribute to Accelerated Loss of Cartilage in Diabetic Fracture Healing. Am J Pathol 2009 175: 1574-1585
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