Type 1 Diabetes Mellitus

Patients with Type 1 diabetes produce no insulin, and their blood glucose levels can be controlled only with daily insulin injections. These patients account for about 10% of all those with diabetes. Previously called juvenile-onset diabetes, Type 1 generally appears before age 30, but it appears most commonly during early adolescence. The disease may appear slightly earlier in females than in males.

The signs and symptoms of Type 1 diabetes seem to begin abruptly. Patients with Type 1 dia­betes are prone to DKA and are at risk for developing vascular complications.

No one fully understands what causes Type 1 diabetes. Some theories suggest a genetic susceptibility linked to an environmental trigger. Genetic studies have shown that a family history of Type 1 diabetes may put a person at risk for developing the disease. Yet, about 80% of children with Type 1 diabetes have no family history of the disease. Human leukocyte antigens, which appear on genes that control immune response, may cause the genetic susceptibility. However, many people have these antigens and never develop diabetes.

Various environmental causes may trigger diabetes in a person who’s genetically susceptible to the disease. For example, children who drink cow’s milk at a young age may be at increased risk for developing Type 1 diabetes because of an autoimmune response to milk proteins. Viruses also seem to play a role in triggering diabetes. The disease appears more commonly in the fall and winter during viral outbreaks, but the time between exposure to the virus and the first signs and symptoms of diabetes makes it difficult to identify the triggering virus.

Islet cell antibodies also have been linked to Type 1 diabetes. Some patients with Type 1 diabetes have islet cell antibodies years before their symptoms begin. These antibodies cause active autoimmunity against beta cells-the cells that produce insulin.

Despite the many theories about the cause of Type 1 diabetes, there’s no way to predict who will develop the disease.

Progression of Type 2 Diabetes

In a patient with Type 2 diabetes, insulin loses its ability to inhibit glucose production, and beta cells are exposed to elevated blood glucose levels. This constant exposure to insulin leaves the beta cells unable to respond to hyperglycemia.

Peripheral insulin resistance occurs when the number of available insulin receptors in muscle and fat cells decreases. This results in higher blood glucose levels, progressively increasing the person’s requirement for insulin secretion. To reseverse the process, the person can lose weight, and to reduce blood glucose levels, she can take oral antidiabetic drugs. If these drugs, in conjunction with weight loss, don’t work effectively, the person may need insulin. She also may need insulin when she’s acutely ill or under stress.

Although the person has high blood glucose levels, she still produces enough insulin to pre vent DKA. However, she may lose fluids and electrolytes-losses that can lead to HHNK syndrome.

People with Type 2 diabetes may experience the same long-term complications as those with Type 1 diabetes. However, they’re particularly at risk for heart disease-the most common cause of death among patients with Type 2 diabetes. The hyperinsulinemia associated with Type 2 diabetes may be an important risk factor in the develop­ment of hypertension, abnormal lipid levels, and atherosclerosis.

Syndrome X is the combination of insulin resistance, hypertension, low high-density lipoprotein cholesterol levels, and increased very-low­density lipoprotein cholesterol levels. By the time most patients are diagnosed with Type 2 diabetes, they’ve had syndrome X for many years. The combined abnormalities of this syndrome increase the chances of angina, myocardial infarction, cerebrovascular accident, and peripheral vascular disease in patients with Type 2 diabetes.