Diabetes Branch - (DB)
Diabetes Branch investigators pursue basic and clinical research designed to better understand the factors that cause diabetes, and/or improve diabetes treatment. All individuals with diabetes have abnormally high blood glucose concentrations and are at risk for similar disease-associated complications like heart disease, blindness, kidney disease, nerve damage, and premature mortality. Blood glucose is normally regulated by insulin, which is only produced by the beta cells of the islets within the pancreas. The disease is generally subdivided into two broad categories called “type 1 diabetes” (T1D) and “type 2 diabetes” (T2D). The two diabetes subtypes appear to have quite different underlying biological mechanisms. T1D is an autoimmune disease; it results when the immune-system kills the insulin-producing beta cells. T2D is caused by several converging defects including resistance of target organs to insulin’s usual action to lower the blood glucose concentration, altered beta cell mass, and ultimately, beta cell dysfunction. T2D is often associated with obesity and other insulin-resistant metabolic states such as pregnancy.
In the laboratory, Diabetes Branch investigators are currently pursuing projects designed to: understand insulin-regulated glucose transport in adipose (fat) and muscle cells, examine the role of dysfunctional adipogenesis in insulin resistance, design and test novel methods for measuring beta cell function and number, understand what regulates beta cell proliferation and differentiation, and understand how immune tolerance induction is altered in the context of autoimmunity. Diabetes Branch investigators are also actively engaged in clinical protocols relevant to both T1D and T2D.
Page last updated: January 21, 2009
