New discovery in preventing diabetic complications

August 23, 2004

A new study sheds light on the response to infection in people with type 2 diabetes. These individuals develop diabetes associated with obesity. Findings from this study revealed that controlling a specific protein produced by the body, known as a cytokine, reduces the expression of other molecules and helps control inflammation. This is significant because many complications associated with diabetes trigger an inflammatory response. Right now, type 2 diabetes affects over 17 million people in the United States and impacts the health industry significantly on economic and individual levels [1].

Tumor necrosis factor (TNF), a type of cytokine, can cause inflammation and damage [2] in soft tissue infections, bite wounds and in periodontal disease. In a recent study published in the Journal of Investigative Dermatology, two groups of lab mice, one normal, the other diabetic, were injected with anaerobic bacteria, a germ present in "approximately one-third of bite wounds and ... associated with the formation of abscesses and with relatively serious infections," [3,4] to determine how type 2 diabetes affects the inflammatory response in surrounding tissue. Results from the tests demonstrated that the presence of diabetes prolongs inflammation. Following infection, the normal mice were able to rapidly resolve the ensuing inflammation within three days whereas the diabetic mice could not.

"It may be particularly important in diabetics to consider the impact that prolonged inflammation might have on the course of events," states contributing author Dr. Dana T. Graves. According to the study, diabetics are particularly susceptible to the detrimental effects of infection associated with inflammatory cytokines. Further, inflammation can often be a precursor to complications such as cardiovascular disease and poor wound healing. Dr. Graves concludes, "If excess TNF in diabetics is inhibited, the tendency for prolonged inflammation is reduced."
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About the Author
Professor Dana T. Graves received his DDS in 1980 from Columbia University and went to Harvard University where he received a Certificate in Periodontology and a Doctor of Medical Sciences in Oral Biology. Dr. Graves is currently a Professor in the Department of Periodontology and Oral Biology at the Boston University School of Dental Medicine, where he has led a research group and taught since 1987. He has authored almost 100 articles published in peer-reviewed journals several of which concern the impact of diabetes on inflammation. Dr. Graves can be reached for questions and interviews at 617-638-8547/4733 or dgraves@bu.edu.

About the Journal of Investigative Dermatology
The Journal of Investigative Dermatology (JID) publishes papers describing original research relevant to all aspects of cutaneous biology and skin disease. The spectrum of interest is indicated by the breadth of the editorial staff and includes biochemistry, biophysics, carcinogenesis, cellular growth and regulation, clinical research, development, epidemiology, extracellular matrix, genetics, immunology, melanocyte biology, microbiology, molecular and cell biology, pathology, pharmacology and percutaneous absorption, photobiology, physiology, and structure. It is published on behalf of the Society for Investigative Dermatology (SID) and the European Society for Dermatological Research (ESDR).

About Blackwell Publishing
Blackwell Publishing is the world's leading, independent society publisher with offices in the US, UK, Japan, Denmark, Australia, and Germany. Blackwell publishes over 700 journals in partnership with more than 550 academic and professional societies.

1 American Diabetes Association, All About Diabetes, 2004
2 Gorman JD, et al: Treatment of ankylosing spondylitis by inhibition of tumor necrosis factor a. New England Journal of Medicine, 346(18): 1349-1356, 2002
3 Edelman S: Importance of glucose control. Med Clin North Am 82:665-687, 1998
4 Zimmet P, Alberti K, Shaw J: Global and societal implications of the diabetes epidemic. Nature 414: 782-787, 2001


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