Diabetes Mellitus

– A disease complex characterized by persistent hyperglycemia caused by insufficient insulin production or resistance to the metabolic action of insulin. Diabetes mellitus (DM) is generally classified as insulin-dependent (IDDM, type I), non-insulin-dependent (NIDDM, type II), or secondary diabetes mellitus.

Causes and Incidence

The precise causal mechanisms in DM are unknown, although genetics and a faulty autoimmune response are thought to play major roles in type I diabetes. Genetics and obesity are risk factors for type II diabetes. Secondary diabetes is caused by underlying primary pathologic abnormalities. DM affects approximately 6% of the U.S. population; it is the leading cause of irreversible blindness and chronic renal failure. Diabetes is found worldwide, and the incidence is increasing rapidly. Type I accounts for 10% to 15% of cases, and the age of onset is primarily childhood or adolescence. Type II accounts for 85% to 90% of cases, and onset generally occurs after age 40. A small number of cases are secondary DM, and the age of onset varies according to the cause of the underlying primary pathologic condition.

Disease Process

Diabetes occurs if the body cannot produce insulin (type I), or if it is unable to use the insulin produced (type II); in either case, the ultimate result is hyperglycemia and impaired glucose transport. Type I diabetes is characterized by a genetic predisposition manifested in one of several human leukocyte antigens. Recent research suggests that the genetic predisposition, coupled with an unknown factor, triggers an ongoing autoimmune process that systematically destroys the beta-cells in the pancreas, thereby interfering with the body’s ability to produce insulin. Type II diabetes involves either a defect in the insulin release sites in the pancreas or a resistance to the action of insulin stemming from a decrease in the number of receptor sites in the peripheral tissues. This type of DM is often associated with obesity.

In both types of DM, the result is interference with glucose transport across cell membranes in peripheral muscle and adipose tissue, leading to faulty oxidation and energy production. Metabolism of fat, carbohydrate, and protein is impaired, as are storage of glycogen in the muscle and liver and storage of fatty acids and triglycerides in adipose tissue. Amino acid cell transport is disrupted. Unrestrained gluconeogenic and glycogenolytic processes in the liver cause overproduction of glucose. As the blood glucose level rises, renal tubules fail to reabsorb all the glucose; this produces glucosuria and osmotic diuresis, with water and electrolyte loss through the urine. Hyperglycemia also damages myelin nerve coverings, leading to neuropathy. Glycosylation (attaching of glucose to protein molecules) in the capillaries causes thickening of the capillary membrane and microangiopathy. Atherosclerotic processes are accelerated, and vessel elasticity diminishes.


Type I
Abrupt onset with polyuria, polydipsia, polyphagia, weight loss, weakness, fatigue, dehydration

Type II
Usually asymptomatic in early stages, with pruritus vulvae a common presenting symptom in women; later manifestations include skin infections, cold extremities, fatigue, blurred vision, delayed healing, and polyuria

Potential Complications

Diabetic ketoacidosis is a common acute complication in type I diabetes. If left untreated, it leads to coma and death. Nonketotic hyperglycemic-hyperosmolar coma is an acute complication in type II diabetes. It is frequently accompanied by seizure activity and has a mortality rate of about 50%. Systemic chronic complications include cardiovascular and peripheral vascular disease, retinopathy, nephropathy, neuropathy, dermopathy, and impotence.

Diagnostic Tests

Fasting blood sugar
.140 mg/dl on two occasions

Glucose tolerance test
.200 mg/dl for 2-hour sample and one other sample after administration of 75 g of glucose

Blood insulin
Absent in type I; normal or elevated in type II

Plasma C-peptide
Absent in type I; normal or elevated in type II


Only for chronic complications such as coronary artery grafts, eye surgery.

Insulin for type I; oral hypoglycemics for type II.

Dietary control aimed at maintaining stable body weight, distributing caloric intake into small, evenly spaced loads, avoiding highfat, high-sugar foods; weight reduction with obesity; regular monitoring of blood sugar; education about disease, complications, medications, diet; counseling, support for adaptation to long-term disease.