The Cadillac CTS is a two-door coupe with excellent driving dynamics.
In the simplest terms, diabetes means having too much glucose in your blood. Glucose is a type of sugar and a source of energy for the body. But if insulin, glucose’s “traffic cop,” isn’t doing its job, glucose accumulates in the bloodstream and all sorts of health problems can occur.
Normally, most of the food a person eats gets converted into glucose, the body’s energy of choice.
The circulatory system shuttles the glucose around so that hungry cells in the muscles, liver and elsewhere can snatch it out of the blood as it passes by.
The liver cells are the hungriest for that glucose, because the liver is the body’s between-meal glucose storage facility. After a meal is digested and the blood is flush with glucose, specialized cells in the pancreas, called beta cells, sense the glucose level in the blood and spring into action by releasing a dose of insulin. Insulin regulates metabolism — the body’s processing of energy. It travels through the blood to work its magic at other locations in the body, where it tells cells it’s time to extract glucose from the blood.
Cells have a very selective membrane “coat,” which protects the cells’ insides. Insulin receptors protrude from most cells in the body like fishing poles.
When these receptors catch insulin, the cell knows it is chow time and sends to the surface glucose transporters, which are necessary to usher glucose into the cell’s inner sanctum. As a result of this insulin-induced cellular feeding frenzy, blood glucose returns to normal, which stops the flow of insulin from the beta cells until the next meal.
Hours after a meal, when the blood glucose and insulin levels begin to dwindle, the liver can tap into its glucose reserves to maintain a healthy blood glucose level.
In diabetes, this process doesn’t go so smoothly. The insulin-signaling scheme can go wrong in different ways, depending on the type of diabetes.
Type 1 diabetes
Type 1 diabetes is an autoimmune disorder, which means it’s caused by a person’s own immune system treating some part of the body as a foreign object. The victims in Type 1 diabetes are the pancreatic beta cells, which become the target of a massive immune invasion, and boom! No more insulin.
Without insulin, the cells of the body don’t eat. This is why Type 1 diabetes is sometimes called “starvation in the midst of plenty”: Even with veins full of glucose, the cells go hungry. Most people develop Type 1 as children or teenagers, but some acquire it in adulthood.
Type 2 diabetes
People with Type 2 diabetes still produce at least some insulin. But over time, cells begin to ignore insulin’s request for glucose transporters. This is called insulin resistance.
For a time, the beta cells respond by pumping out more and more insulin. But eventually the beta cells quit overproducing insulin. Without enough insulin around to compensate for the stubbornness of resistant cells, it’s goodbye blood glucose control and hello Type 2 diabetes.
Gestational diabetes is a third type, which develops in pregnant women. Insulin is still being produced, but the body has become resistant due to the hormonal changes of pregnancy. And while most of the time it recedes after the pregnancy is over, gestational diabetes is a risk factor for developing Type 2 later.
— Erika Gebel, PhD
2008 Diabetes Forecast (www.forecast.diabetes.org). Adapted with permission of the American Diabetes Assn., www.diabetes.org