Nearly 21 million Americans suffer from type 2 diabetes, and every year 800,000 more are diagnosed. Considering the growing numbers, scientists are trying to fit together the disease’s disparate puzzle pieces. People who acquire it are typically obese, suffer from chronic inflammation and are resistant to insulin, the hormone that removes sugar from the blood and stores it as energy. For years no one has known exactly how the three characteristics are related, if at all. But a handful of recent studies suggest that they are inextricably linked through the actions of specific inflammatory immune cells and a master genetic switch–and the hope is that an understanding of the relations could open the door to new therapeutic opportunities.
Several decades ago scientists noticed that people with type 2 diabetes have overly active immune responses, leaving their bodies rife with inflammatory chemicals. In the early 1990s researchers at Harvard University pinpointed one major immune player as TNF-alpha, a chemical secreted by immune cells; such compounds are generally referred to as cytokines. They found high levels of the cytokine in the fat tissue of rats with type 2 diabetes, and when they bred obese rats that could not make the cytokine, diabetes did not develop in the animals. Researchers have since shown that TNF-alpha–and, more generally, inflammation–activates and increases the expression of several proteins that suppress insulin-signaling pathways, making the human body less responsive to insulin and increasing the risk for insulin resistance.
