Diabetes and hyperglycemia create a proinflammatory microenvironment that progresses to microvascular complications such as nephropathy, retinopathy, and neuropathy. Diet- induced insulin resistance is a potential initiator of this change in type 2 diabetes which can increase adipokines and generate a chronic low-grade inflammatory state. Advanced glycation end-products and its receptor, glycation end-productsAGE receptor axis, reactive oxygen species, and hypoxia can also interact to worsen complications. Numerous efforts have gained way to understanding the mechanisms of these modulators and attenuation of the inflammatory response, however, effective treatments have still not emerged. The complexity of inflammatory signaling may suggest a need for multi-targeted therapy.This review presents recent findings aimed at new treatment strategies.
- Advanced glycation end-products
- Diabetes mellitus
- Inflammatory cytokines
- Microvascular complications
- Oxidative stress
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism