Diabetes, Inflammation, Proinflammatory Cytokines, and Diabetic Nephropathy

Juan F Navarro,Carmen Mora

doi:10.1100/tsw.2006.179

Abstract

Diabetes and its complications have become a public health problem. Diabetic nephropathy is the main cause of renal failure. In spite of our higher knowledge on this complication, the intimate mechanisms leading to the development and progression of renal injury are not yet fully known. Activated innate immunity and inflammation are relevant factors in the pathogenesis of diabetes. Moreover, inflammation, and more specifically proinflammatory cytokines and other molecules with a relevant role within the inflammatory process, may be critical factors in the development of microvascular diabetic complications, including nephropathy. This new pathogenic perspective may lead to important new therapeutic considerations and new therapeutic goals for the treatment of diabetic nephropathy.

Highlights

Diabetes mellitus, specially type 2 diabetes, is a public health problem that has reached the range of epidemic due to the rapidly increasing rates of the disease throughout the world
Several cross-sectional studies in the general population, as well as in nondiabetic subjects, in individuals with impaired glucose tolerance (IGT)/impaired fasting glucose (IFG) and in newly diagnosed or established type 2 diabetic patients have shown that acute-phase reactants and proinflammatory cytokines, such as C-reactive protein (CRP), sialic acid, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6), are positively correlated with measures of insulin resistance[4,5,6,7,8,9]
The pathogenic vision of diabetes mellitus has substantially changed in the last years

Summary

INTRODUCTION

Specially type 2 diabetes, is a public health problem that has reached the range of epidemic due to the rapidly increasing rates of the disease throughout the world. Several studies with the recently introduced thiazolidinediones have reported a significant improvement in insulin sensitivity[22] as well as a decrease in the risk of progression to diabetes in subjects with a known high risk for developing this disease[23]. In addition to their actions as PPAR-γ agonists, glitazones have anti-inflammatory effects with inhibition of cytokine production, macrophage activation, and reduction of the levels of inflammatory markers such as CRP[24,25,26]. Activated innate immunity and inflammation are relevant factors in the pathogenesis of diabetes, with convincing data that type 2 diabetes includes an inflammatory component[6,27]

PROINFLAMMATORY CYTOKINES AND DIABETIC NEPHROPATHY

Findings

CONCLUSIONS