The role of exercise in treating type II non-insulin dependent diabetes.

The majority of the 7+ million people with diabetes in this country are non-insulin dependent diabetic (NIDDM). Over eighty percent of all NIDDM patients are obese. In addition, a growing number of Americans have fasting blood glucose levels which would classify them as border-line diabetic.

While insulin-dependent diabetes (IDDM) results from the inability of a person's pancreas to produce the hormone insulin, NIDDM is associated with elevated insulin levels, resistance to the hormone, and poor glucose tolerance.

It is still debatable in the scientific community which comes first- does the insulin resistance associated with NIDDM cause obesity, or does obesity result in insulin resistance and later the development of NIDDM. Whatever the case, both types of NIDDM are to a large degree preventable and treatable through diet and exercise.

Insulin's primary role is to lower blood glucose levels. The two major target tissues of insulin are skeletal muscle and adipose (fat) tissue. Whenever someone eats a meal containing carbohydrates that food is digested and converted into glucose. The rise in blood glucose causes the release of insulin from the pancreas and the resultant uptake of glucose into muscle and fat cells.

Along with diet, exercise plays a key role in NIDDM treatment and in determining one's sensitivity to insulin. Fat cells contain only one type of glucose transport protein (a glut-4 transporter) which respond to insulin and increase glucose transport into the fat cell whenever insulin levels go up. Unfortunately, most of the glucose that enters the fat cell are converted to triglycerides and stored as fat.

Muscle on the other hand has two different types of glucose transport proteins, one insulin regulatable (a glut-4 transporter) and one which is insulin independent (a glut-1 transporter). The glut-1 transporter functions in the basal state (between meals), whenever the muscle is active, and for a period of time after exercise. This increased glucose transport which is stimulated by activity and exercise - by the glut-1 transporter and independent of insulin - is what improves glucose tolerance and insulin sensitivity in individuals who exercise regularly.

Because glut-1 transporters exist in IDDM individuals and require no insulin to transport glucose into the muscle cells, IDDM patients who exercise require a lower insulin dose than sedentary ones.

So now you can begin to understand how your workouts are not only improving you blood glucose and lipid levels they are modifying the activity of your glut-1 transporters and improving your blood glucose regulation and insulin sensitivity.

An added benefit of improved insulin sensitivity, and lower basal and post-meal insulin levels, is that you'll not only have less glucose transported into your fat cells and less conversion into fat, but you will also have a lower activity of the enzyme lipoprotein lipase and less of a stimulus for TG storage in your fat cells. But that is another story for another post.