Diabetes is a proinflammatory state: a translational perspective

Abstract

The diabetic state confers an increased propensity to accelerated atherogenesis. Inflammation is pivotal in atherosclerosis; in addition to the established risk factors, inflammation appears to play a pivotal role in diabetes and its complications. Evidence for increased inflammation includes: increased levels of plasma C-reactive protein, the prototypic marker of inflammation; increased levels of plasminogen-activator inhibitor; increased monocyte superoxide and proinflammatory cytokine release (IL-1, IL-6 and TNF-α); increased monocyte adhesion to endothelium; increased NF-κB activity; and increased Toll-like receptor 2 and 4 expression and activity in diabetes. Thus, it appears that both Type 1 and Type 2 diabetes are proinflammatory states and that these could contribute to increased diabetic vasculopathies.

Keywords::

• atherosclerosis
• C-reactive protein
• diabetes
• inflammation
• Toll-like receptor

Financial & competing interests disclosure

Studies cited in this review were funded by the NIH, Juvenile Diabetes Foundation and American Diabetes Association. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.