The reasons that type 2 diabetes occurs are different from those that trigger type 1 diabetes. Unlike people with type 1 diabetes, who become unable to produce insulin, people with type 2 diabetes produce insulin. But, either the body does not respond to insulin’s action (it’s resistant) or there is just not enough insulin to go around-or both. Either problem leads to the same outcome: insulin can’t deliver glucose to the cells that need it, and there’s too much glucose in the blood.

Virtually all cells in the body contain special proteins called receptors that bind to insulin. They work like a lock and key.

In order for glucose to enter the cell, insulin (the key) must first fit into the insulin receptor (the lock). But for some reason, in some people with type 2 diabetes, there is a faulty lock, or insulin receptor. The key doesn’t open the lock, and glucose is shut out of the cell. And in some people with type 2 diabetes, there are not enough locks, or insulin receptors, on the cells to allow enough glucose to enter. But for most people with diabetes, it’s not so much that the key doesn’t fit the lock, but that insulin doesn’t work properly. In rare cases, the insulin is mutated, or built incorrectly, and does not fit the insulin receptor.

Initially, the pancreas is able to produce enough insulin to overcome the resistance. But over the course of several years, the beta cells in the pancreas are no longer able to produce enough insulin or it is released too slowly. Without enough insulin to meet the body’s needs, glucose levels rise and diabetes results. Scientists do not know why the pancreas does not function well in these people. Some believe that the system that controls glucose levels in the blood and tells the pancreas to make more insulin does not function properly. Others think that the pancreas, after many years of working overtime to overcome insulin resistance, simply begins to “burn out.”

Although researchers do not fully understand why type 2 diabetes develops, they have uncovered many factors that may contribute to the disease.

Genetics
Genetics also appears to play a role in how type 2 diabetes develops. Like type 1 diabetes, type 2 diabetes also appears to run in families, and it is most likely due to the inheritance of certain genes.  The link to genetics seems even stronger in type 2 diabetes than in type 1 diabetes. If a person with type 1 diabetes has an identical twin, there is a 25 to 50 percent chance that the twin will develop diabetes. But if a person with type 2 diabetes has an identical twin, there is a 60 to 75 percent chance that the person will develop diabetes.

More evidence for the role of genes in type 2 diabetes comes from studying certain ethnic groups. Compared with Caucasians, African Americans,  Asian Americans,  Hispanic Americans (except Cuban Americans), and Native Americans all get type 2 diabetes more often. Native Americans have the highest rate of type 2 diabetes in the world. Hispanic groups, such as Mexican Americans,  that share genes with Native American groups (where there has been cultural mixing) have a higher rate of type 2 diabetes than Hispanic groups,  such as Cuban Americans, where less intercultural contact has occurred.

Researchers have not yet isolated a single “type 2 diabetes” gene, but they are finding several that may contribute to type 2 diabetes. For example, researchers have identified a protein called PC-1 that shuts down the insulin receptor,  creating insulin resistance. This protein is prevalent in most people with type 2 diabetes, compared with people without diabetes. For some reason, too much of the inhibitor protein is made in some people, and the insulin receptor cannot do its job properly, which can lead to insulin resistance.

Researchers believe that the genes that lead to obesity may also play a role in diabetes. In mice, scientists have identified a gene they called the obese gene. The obese gene appears to regulate body weight by making proteins that affect the center in the brain that tells you whether you’re full or hungry. When the obese gene is mutated,  the mice become obese and develop type 2 diabetes.