In the absence of insulin, glucose in the bloodstream cannot be transferred into cells as it normally would, resulting in high glucose levels in the bloodstream and a state of “starvation” within cells. The kidneys filter the excess glucose out of the blood, causing increased urination, thirst, and dehydration. Starving cells, no longer able to use glucose for energy, begin to use fat, resulting in loss of body fat and the production of ketones (chemical by-products of fat metabolism). If not treated (with insulin) in time, the combination of high blood glucose, high levels of ketones, and dehydration can lead to a very serious condition called diabetic ketoacidosis and, potentially, death.
Some people with Type 1 diabetes experience a “honeymoon” period after diagnosis, during which their pancreas regains the ability to produce insulin, and they require little or no injected insulin, but this generally lasts only a short time. Within a few months, most people have very little insulin-producing capacity and require an outside source of insulin.
Type 2 diabetes
Type 2 diabetes is much more common than Type 1 and has a stronger genetic link. (If one identical twin develops Type 2 diabetes, there is a 90% chance that the other one will also.) Symptoms of high blood glucose are less pronounced in Type 2 diabetes compared to Type 1 diabetes; because of this, diagnosis often occurs many years after diabetes initially develops. However, the damage starts even in the absence of acute symptoms: Blood glucose levels above normal are known to increase a person’s chances of eventually developing heart disease and other complications of diabetes.
Unlike Type 1 diabetes, Type 2 diabetes is not caused by an autoimmune attack. Instead, there are usually two underlying problems: insulin resistance and inadequate insulin production. Insulin resistance is when the cells of the body have a decreased response to insulin. Under normal circumstances, when blood glucose levels are high (after eating, for example), the pancreas releases insulin into the bloodstream. Insulin then interacts with muscle cells, fat cells, and other tissues, allowing them to transport glucose into the cells to be burned for energy or stored for use later.
In insulin resistance, these important messages do not get through. Remember playing “telephone” as a child, when one person would whisper a word to the person next to them, and that person would whisper what they heard to the next person, and so on down the line? By the time it got to the end of the line, the word had usually mutated to something completely unrecognizable. A similar breakdown in communication is thought to occur in insulin resistance, where the signal from insulin becomes garbled, and the cell does not respond normally, taking up much less glucose than normal.
When blood glucose levels remain high, the pancreas continues to secrete more insulin to compensate for its decreased effectiveness, and eventually, blood glucose returns to the normal range. Over time, however, the pancreas loses the ability to produce enough extra insulin to compensate for insulin’s decreased effectiveness, and blood glucose levels remain high. At this point, a person might be diagnosed with diabetes or prediabetes, depending on his blood glucose level at the time of testing.
The liver also plays a key role in regulating blood glucose level. It releases glucose to the bloodstream when the blood glucose level is low, and it stores glucose when the level is high. When the blood glucose level is high, insulin has the important role of signaling the liver to turn off glucose production and start storing extra glucose. But if a person is insulin resistant, the liver does not respond normally to insulin, so it continues to release glucose to the bloodstream even if the blood glucose level is already elevated, making it even higher.