Immune System and Latent Autoimmune Diabetes

In people with diabetes mellitus (DM), the risk of infection is higher. Diabetic people are also more prone than nondiabetic patients to have a complicated course with several of these infections. To develop systemic insulin resistance, hyperglycemia disrupts the normal operations of the circulatory system, gastrointestinal tract, pancreatic beta cells, liver, and skeletal muscles. Immune cells become dysfunctional in a hyperglycemic environment.

Adult-onset autoimmune diabetes (LADA) is a kind of autoimmune diabetes that does not require insulin for glycemic control for at least the first six months after diagnosis. Both type 1 and type 2 diabetes mellitus share genetic, immunologic, and metabolic characteristics (DM). This disease is more complex than young-onset autoimmune diabetes, with clinical and metabolic similarities to both type 2 and type 1 diabetes. Patients with LADA have extremely varied -cell destruction, varying degrees of insulin resistance, and heterogeneous islet autoantibody titer and pattern, implying various pathophysiological mechanisms that may explain the heterogeneous symptoms of LADA.

• Immunometabolism
• Immune Cell Infiltration and Inflammation
• Epidemiology of Latent Autoimmune Diabetes
• Pathophysiology of Latent Autoimmune Diabetes
• Evaluation and Management of Latent Autoimmune Diabetes