Advanced Glycation End Products and Inflammation in Type 1 Diabetes Development

Type 1 diabetes (T1D) is an autoimmune disease in which the beta-cells of the pancreas are attacked by the host's immune system, ultimately resulting in hyperglycemia. It is a complex multifactorial disease postulated to result from a combination of genetic and environmental factors. In parallel with increasing prevalence of T1D in genetically stable populations, highlighting an environmental component, consumption of advanced glycation end products (AGEs) commonly found in in Western diets has increased significantly over the past decades. AGEs can bind to cell surface receptors including the receptor for advanced glycation end products (RAGE). RAGE has proinflammatory roles including in host-pathogen defense, thereby influencing immune cell behavior and can activate and cause proliferation of immune cells such as islet infiltrating CD8(+) and CD4(+) T cells and suppress the activity of T regulatory cells, contributing to beta-cell injury and hyperglycemia. Insights from studies of individuals at risk of T1D have demonstrated that progression to symptomatic onset and diagnosis can vary, ranging from months to years, providing a window of opportunity for prevention strategies. Interaction between AGEs and RAGE is believed to be a major environmental risk factor for T1D and targeting the AGE-RAGE axis may act as a potential therapeutic strategy for T1D prevention.

Automated summary

Type 1 diabetes (T1D) is an autoimmune disease caused by a combination of genetic and environmental factors. The consumption of advanced glycation end products (AGEs) found in Western diets is believed to be a major environmental risk factor for T1D, as it interacts with the receptor for advanced glycation end products (RAGE). The progression of T1D varies in individuals, providing an opportunity for prevention strategies. Targeting the AGE-RAGE axis may be a potential therapeutic strategy for T1D prevention.