Diabetes mellitus results primarily from inadequate secretion of insulin or the inability of tissues to respond to insulin.

Insulin-dependent diabetes mellitus (DDM), also call type 1 diabetes mellitus, is caused by diminished insulin secretion. It most commonly develops in young people, and it is not clear if heredity plays a major role in its onset, but viral infection of the pancreatic islets may be involved. Noninsulin-dependent diabetes mellitus (NIDDM), also call type II diabetes mellitus, results from the inability of the tissues to respond to insulin. NIDDM usually develops in older people, although the age of onset varies tremendously, and it apparently is in part hereditary.

Major symptoms associate with both types of diabetes mellitus are the consequence of the abnormal metabolism of nutrients, which is caused by diminished insulin secretion or a decreased number of insulin receptors.

In patients with IDDM, nutrients are absorbed from the intestine after a meal, but skeletal muscle, adipose tissue, the liver, and other target tissues do not readily take glucose into their cells. Consequently, blood levels of glucose increase dramatically. Even though blood glucose levels increase, the glucose does not enter cells, and fat and protein catabolism increases to provide energy. Wasting a body tissue is common in patients with untreated IDDM in spite of a high food intake. Food intake can be excessive because, without insulin, glucose does not enter the cells of the satiety center, resulting in an increased appetite. If blood sugar levels are high enough, glucose is also excreted in the urine, which results in an increase of urine volume. Normally urine does not contain glucose. Although other disorders can result in glucose in the urine, the presence of glucose in the urine is taken as strong evidence of diabetes mellitus and that further diagnostic tests are required.

Rapid urine production occurs as a result of the elevated concentration of blood glucose and leads to dehydration. The rapid loss of water in the urine increases the osmotic concentration of blood, which causes an increase in the sensation of thirst. The resulting ionic imbalances cause neurons to malfunction and result in diabetic coma in severe cases. Polyurea (increased urine volume), polydipsia (increased thirst), and polyphagia (increased appetite) are major symptoms of IDDM.

Acidosis is caused by rapid fat catabolism that results in increased levels of acetoacetic acid, which is converted to acetone and beta-hydroxybutyric acid. These three substances collectively are referred to as ketone bodies. The presence of excreted ketone bodies in urine and in expired air ("acetone breath") is used as one diagnostic test for diabetes mellitus.

Diabetes mellitus often is treated by the administration of insulin by injection. Insulin is extracted from sheep or pork pancreatic tissue and is purified for use by diabetic patients. Genetic engineering currently is used to synthesize human insulin. A gene for human insulin is placed in the bacterium Escherichia coli so the E. coli synthesizes human insulin, The insulin is extracted from the bacterial cultures and packaged for use by diabetic patients. In some cases, diabetes mellitus can be treated by administering drugs that stimulate beta cells to secrete more insulin. This treatment is effective only if an adequate number of functional beta cells is present in the pancreatic islets.

NIDDM is more common than IDDM. The reduced number of receptors for insulin results in elevated blood glucose levels. Obesity is common, although not universal, in patients with NIDDM. Elevated blood glucose levels cause fat cells to convert glucose to fat, even though the rate at which adipose cells take up glucose is impaired. The poor use of nutrients leads to lethargy, fatigue, and periods of irritability. The elevated blood glucose levels lead to recurrent infections and prolonged wound healing. Damage to blood vessels results in damage to the retina of the eye, damage to the kidney, and an increased chance of heart attack and stroke. Prolonged wound healing, recurrent infections, damage to blood vessels, and reduced nerve function are long-term symptoms also seen in patients with NIDDM and IDDM.

Patients with NIDDM do not suffer the sudden large increases of blood glucose and severe tissue wasting seen in IDDM because, although the reduced uptake of glucose results from inadequate insulin receptors, a slower rate of glucose uptake does occur.

Glucose tolerance tests are used to diagnose diabetes mellitus. In general, the test involves feeding the patient a large amount of glucose after a period of fasting. Blood samples are collected for a few hours, and a sustained increase in blood glucose levels strongly indicates that the person is suffering from diabetes mellitus.

Too much insulin or too little food intake after an injection of insulin by a diabetic patient causes insulin shock. The high levels of insulin cause target tissues to take up glucose at a very high rate. As a result, blood glucose levels rapidly fall to a low level. Because the nervous system depends on glucose as its major source of energy, neurons malfunction because of a lack of metabolic energy. The result is a series of nervous system responses that include disorientation, confusion, and convulsions.

Recent reports indicate that damage to blood vessels and reduced nerve function can be reduced in diabetic patients suffering from either IDDM or NIDDM by keeping the blood glucose well within normal levels at all times. However, keeping the blood glucose levels within the normal range at all times requires increased attention to diet, frequent blood glucose testing, and increased chance of suffering from low blood glucose levels, which lead to symptoms of insulin shock. A strict diet and routine exercise are often effective components of a treatment strategy for diabetes mellitus, and in many cases diet and exercise are adequate to control NIDDM.

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