The increased prevalence of type 2 diabetes parallels the increased prevalence of obesity. Abdominal obesity contributes to insulin resistance. To overcome the insulin resistance, the pancreas makes more insulin, keeping the glucose in the normal range. Eventually, the pancreas will fail, resulting in elevated levels of blood glucose. Thus, to develop type 2 diabetes, an individual must have a defect in insulin sensitivity with an accompanying defect in insulin secretion. In the early stages of the disease, glucose can be controlled with appropriate therapeutic lifestyle changes aimed at lowering insulin resistance. As the disease progresses, one has to use medications. Insulin secretagogues increase insulin levels, whereas insulin sensitizers, such as metformin and thiazolidinediones, decrease insulin resistance. The defect in insulin secretion is progressive, and eventually, almost every patient needs exogenous insulin, which may be delayed with appropriate lifestyle changes. Insulin resistance is associated with a clustering of metabolic abnormalities called the insulin-resistance syndrome, which is a component of the metabolic syndrome. Insulin-resistance syndrome includes obesity, hypertension, dyslipidemia, and elevated levels of plasminogen activator inhibitor type 1. These abnormalities increase the risk of cardiovascular disease. Of people with type 2 diabetes, 70% die from premature cardiovascular disease. Prevention of the complications of diabetes requires good control of not only blood glucose but also other manifestations of the insulin-resistance syndrome, including hypertension and lipid abnormalities.