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Autoimmune Dis. 2012; 2012: 346501.
Published online Aug 12, 2012. doi:  10.1155/2012/346501
PMCID: PMC3424633
Improved Metabolic Control in Diabetes, HSP60, and Proinflammatory Mediators
Claudio Blasi, 1 * Eunjung Kim, 2 and Anne A. Knowlton 3
1Centro Diabete, ASL RMB-1D, L.go T. Solera n.7, Rome, Italy
2St. Mary's Hospital of Daejeon Catholic University, Clinical Research Institute, Daeheung-dong, Daejeon, Republic of Korea
3Cardiovascular Division, Department of Medicine and Department of Medical Pharmacology, UC Davis Health Systems, Sacramento, CA 95817, USA
*Claudio Blasi: diabcb/at/
Academic Editor: Kamal D. Moudgil
Received March 15, 2012; Revised May 3, 2012; Accepted May 31, 2012.
The diabetes-atherosclerosis relationship remains to be fully defined. Repeated prolonged hyperglycemia, increased ROS production and endothelial dysfunction are important factors. One theory is that increased blood levels of heat shock protein (HSP)60 are proinflammatory, through activation of innate immunity, and contribute to the progression of vascular disease. It was hypothesized that improvement of diabetes control in patients presenting with metabolic syndrome would lower HSP60, and anti-HSP60 antibody levels and decrease inflammatory markers. Paired sera of 17 Italian patients, before and after intensive treatment, were assayed for cytokines, HSP60 and anti-HSP60 antibodies. As expected, intensive treatment was associated with a decrease in HgbA1C (P < 0.001) and BMI (P < 0.001). After treatment, there was a significant decrease in IL-6 (P < 0.05). HSP60 levels were before treatment −6.9 + 1.9, after treatment −7.1 + 2.0 ng/mL (P = ns). Overall HSP60 concentrations were lower than published reports. Anti-HSP60 antibody titers were high and did not decrease with treatment. In conclusion, improvement of diabetic control did not alter HSP60 concentrations or antiHSP60 antibody titers, but led to a reduction of IL-6 levels.
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