Insulin Resistance

Overview :

To understand insulin resistance, it may be helpful for the reader to have a brief account of the way insulin works in the body. After a person eats a meal, digestive juices in the small intestine break down starch or complex sugars in the food into glucose, a simple sugar. The glucose then passes into the bloodstream. When the concentration of glucose in the blood reaches a certain point, the pancreas is stimulated to release insulin into the blood. As the insulin reaches cells in muscle and fatty (adipose) tissues, it attaches itself to molecules called insulin receptors on the surface of the cells. The activation of the insulin receptors sets in motion a series of complex biochemical signals within the cells that allow the cells to take in the glucose and convert it to energy. If the pancreas fails to produce enough insulin or the insulin receptors do not function properly, the cells cannot take in the glucose and the level of glucose in the blood remains high.

The insulin may fail to bind to the insulin receptors for any of several reasons. Some persons inherit a gene mutation that leads to the production of a defective form of insulin that cannot bind normally to the insulin receptor. Others may have one of two types of abnormalities in the insulin receptors themselves. In type A, the insulin receptor is missing from the cell surface or does not function properly. In type B, the person's immune system produces autoantibodies to the insulin receptor.

In the early stages of insulin resistance, the pancreas steps up its production of insulin in order to control the increased levels of glucose in the blood. As a result, it is not unusual for patients to have high blood sugar levels and high blood insulin levels (a condition known as hyperinsulinemia) at the same time. If insulin resistance is not detected and treated, however, the islets of Langerhans (the insulin-secreting groups of cells) in the pancreas may eventually shut down and decrease in number.