Introduction to Diabetes and Obesity

Diabetes and obesity have reached epidemic proportions globally, and they are a major contributor to the development of many pathological processes including hypertension, hyperlipidemia, cardiovascular diseases, and certain types of cancer. Increased consumption of more energy-dense, nutrient-poor diets with high levels of carbohydrates and saturated fats, combined with reduced physical activity, has led to currently observed high rates of diabetes and obesity. A strong relationship exists between diabetes and obesity, with fat tissue playing an important role in diabetes, a disease characterized by hyperglycemia, insulin hyposecretion, and insulin resistance. The resistance manifests primarily as impaired ability of the muscle tissue to take up glucose and of the liver to curb glucose output in response to insulin. Eventually, pancreatic beta cell insufficiency leads to overt diabetes. Obesity is often accompanied by inflammation and insulin resistance and is a preamble to the development of type 2 diabetes. Studies of the last two decades revealed that insulin resistance is multifactorial and coexists with elevated levels of circulating insulin, fatty acids, and oxidative radicals and with low-level inflammation. The first three factors individually cause insulin resistance when applied to rodents or cell cultures. In addition, recent data have revealed that the plasma concentration of inflammatory mediators, such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), is elevated in the insulin-resistant states of obesity and type 2 diabetes, raising questions about the mechanisms underlying inflammation in these two conditions. It is also intriguing that an increase in inflammatory cytokines or indices predicts the future development of diabetes and obesity. Novel approaches in preventing and managing overweight/obesity and diabetes must be developed in order to stop the invasion of these two twin epidemics.