Updated April 26, 2005

Insulin Therapy for Type 2 Diabetes

by Virginia Peragallo-Dittko, R.N., B.C.-A.D.M., M.A., C.D.E.

Al just couldn’t believe what he was hearing. “Insulin for me? But I exercise almost every day. I eat so much less than I used to, and I never skip my pills. What more can I do? Why has my diabetes gotten worse?”

Every number in Al’s blood glucose log is over 200 mg/dl and his glycosylated hemoglobin reading (or HbA1c, a measure of long-term blood glucose control) has slowly increased from 7.2% to over 10%. (The American Diabetes Association recommends aiming for an HbA1c less than 7%.) You can empathize with his frustration; he’s trying to do his part to keep his blood glucose within range, but his HbA1c keeps increasing. Why have his blood glucose readings gotten higher?

To understand the answer to this question, it helps to first understand why our bodies need insulin. Insulin is a hormone secreted by the beta cells of the pancreas that helps regulate the way the body uses one of its main sources of fuel, glucose. Its main job is to allow glucose in the blood to enter the cells of the body, where the glucose can be used for energy. Insulin also controls the rate at which glucose is produced and secreted by the liver. Glucose is stored in the liver in the form of glycogen. When a person’s blood glucose level drops, the liver converts glycogen to glucose and releases this glucose into the bloodstream. When there is enough glucose in the bloodstream, insulin secreted by the pancreas signals the liver to shut down glucose production. In people who do not have diabetes, the pancreas continually measures blood glucose levels and responds by secreting just the right amount of insulin—whether it is during the night, before meals, or during periods of stress. However, in people with Type 2 diabetes, there is a flaw in the system.

The two main problems behind Type 2 diabetes are insulin resistance and inadequate insulin secretion because of a defect in the beta cells. When a person has insulin resistance, the cells of his body are unable to take as much glucose from the bloodstream as they should, even when there’s a lot of insulin in the bloodstream. That is, the cells resist the insulin. On top of that, the liver may continue to secrete a lot of glucose into the bloodstream even when it isn’t needed. So insulin resistance can lead to higher blood glucose levels, especially following meals, and this causes the pancreas to secrete more insulin to compensate. At first, this may keep blood glucose levels within the normal range, but eventually the overworked beta cells produce less and less insulin.

So what happened to Al? His beta cells no longer secrete enough insulin for his needs. He could exercise like a professional athlete, follow a restricted diet, and follow every guideline for self-management, and his blood sugar levels would remain high simply because his pancreas cannot make enough insulin.

It’s not his fault…
Al is upset because he has tried hard to keep his blood glucose level within his target range, and he feels as though he has failed. But the truth is that Al didn’t fail; his pancreas did. In fact, his efforts at exercise and healthy eating probably created an environment that prolonged the life of his beta cells. Research confirms that the nature of Type 2 diabetes involves the progressive loss of beta-cell function. Taking the burden of producing lots of insulin off the beta cells by treating insulin resistance through weight loss, healthy eating, exercise, and certain medicines is clearly effective. In fact, the research devoted to the delay and prevention of Type 2 diabetes has shown the importance of preserving beta-cell function as well as reducing insulin resistance.

For years, people worried that one group of pills used to treat diabetes, the sulfonylureas, might be contributing to the decline of the beta cells. These pills, namely glyburide (DiaBeta, Glynase, Micronase), glipizide (Glucotrol, Glucotrol XL), and glimepiride (Amaryl), work by stimulating the pancreas to secrete more insulin. But research has proved that it is the beta-cell defect and progressive nature of Type 2 diabetes, not overstimulation by these pills, that leads to the decline in insulin production by the pancreas. Some people have a robust pancreas that continues to produce insulin when stimulated by these pills, and they never require injections of insulin. But if your pancreas no longer makes insulin, these pills will not help you.

Virginia Peragallo-Dittko is a diabetes nurse specialist and Director of the Diabetes Education Center at Winthrop-University Hospital in Mineola, New York.

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