Genetic and environmental risk elements impact inflammation, autoimmunity, and metabolic stress. These states affect β-cell mass and/or characteristic such that insulin degrees are ultimately not able to respond sufficiently to insulin demands, leading to hyperglycemia ranges enough to diagnose diabetes. In some cases, genetic and environmental risk factors and gene-environment interactions can directly affect β-cell mass and/or function. Regardless of the pathophysiology of diabetes, chronic excessive blood glucose stages are related to microvascular and macrovascular complications that increase morbidity and mortality for people with diabetes. This model positions β-mobile destruction and/or dysfunction as the necessary not unusual element to all types of diabetes.