Improved metabolic control in diabetes, HSP60, and proinflammatory mediators

Claudio Blasi, Eunjung Kim, Anne A Knowlton

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Article number346501
JournalAutoimmune Diseases
Volume1
Issue number1
DOIs
StatePublished - 2012

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Anti-Idiotypic Antibodies
Interleukin-6
Therapeutics
Chaperonin 60
Vascular Diseases
Innate Immunity
Hyperglycemia
Atherosclerosis
Cytokines
Antibodies
Serum

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology and Microbiology (miscellaneous)
  • Immunology

Cite this

Improved metabolic control in diabetes, HSP60, and proinflammatory mediators. / Blasi, Claudio; Kim, Eunjung; Knowlton, Anne A.

In: Autoimmune Diseases, Vol. 1, No. 1, 346501, 2012.

Research output: Contribution to journalArticle

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