1.1. TYPE I (IDDM)
There are two major types of diabetes, Type I and Type II.
Type I, known as insulin-dependent diabetes mellitus (IDDM), is considered an autoimmune disease because the pancreatic cells that produce insulin, the ß-cells, are destroyed by the body’s own immune system. The pancreas then produces little or no insulin. To live, the person with IDDM needs daily injections of insulin. At present, scientists do not know exactly what causes the body’s immune system to attack the ß-cells, but they believe that both genetic factors and viruses may be involved (see reference 2). IDDM accounts for approximately 10 % of diagnosed diabetes in the United States.
IDDM usually develops in children or young adults, although the disorder can appear at any age. Symptoms of IDDM usually develop over a short period, although ß-cell destruction can begin months, or even years, earlier. Symptoms include increased thirst and urination, constant hunger, weight loss, blurred vision, and great tiredness. If not diagnosed and treated with insulin, the person can lapse into a life-threatening coma.
1.2. TYPE II (NIDDM)
Type II diabetes, also known as non-insulin-dependent diabetes mellitus (NIDDM), is much more common than Type I diabetes, affecting 80-90% of all persons with diabetes. (Thus, we use ‘diabetes’ and ‘NIDDM’ interchangeably unless there is a need to differentiate them clearly.) Initially, NIDDM is often of gradual onset in middle age. However, later stages of this disease are very severe, resulting in various long-term complications, such as kidney disease, heart disease, eye disease, nerve disease and others. These complications make diabetes a leading cause of death.
The symptoms of NIDDM can be vague to diagnose. The symptoms may include fatigue, nausea, frequent urination (particularly at night), and unusual thirst. Frequent urination is one way the body gets rid of excess glucose, and this loss of fluid leads to thirst.
Obesity is an important factor in NIDDM. Also, NIDDM develops more often in genetically predisposed individuals.
The pathological changes in the pancreatic islets of patients with NIDDM are not always apparent. Many patients with NIDDM have normal to high plasma insulin levels. In these individuals, diabetes arises not from a shortage of insulin, but may arise from defects in the molecular machinery that mediates the action of insulin on its target cells.
In other words, NIDDM is not caused by ß-cell destruction but by other mechanisms, such as insulin resistance (see reference 3), related to downregulation of insulin receptors, defects in insulin secretion from the pancreatic ß-cells and other changes to the glucose transporter system.
1.3. COST AND TREATMENT OPTIONS
Diabetes, especially NIDDM, also has an enormous financial impact on society. In the U.S., the total economic cost of diabetes (comprised of medical care and lost productivity) was estimated to be $92 billion in 1992. The American Diabetes Association estimated the direct medical costs of diabetes at $45.2 billion. That included the cost of blood-sugar tests and insulin as well as the costs related to kidney failure, retinopathy and other diabetes-related illnesses. The American Diabetes Association also said the indirect costs of diabetes, such as lost productivity and premature death, equal $46.6 billion. World estimates would place the total economic cost of NIDDM conservatively at over 1 trillion dollars.
Presently, no oral hypoglycaemic agent or combination drug therapy exists to treat NIDDM patients without toxicity or side effects. Insulin treatment also provides symptomatic relief rather than a cure. When treatment with insulin is stopped in patients with severe NIDDM, blood glucose levels increase.
It means that most of the current options provide symptomatic or temporary treatment rather than a permanent solution. The void within the art of diabetic treatments in the prevention and/or long term cure of diabetes has not yet been filled.
1.4. ELEOTIN: PROMISING NEW TREATMENT FOR DIABETES
This report investigates some preliminary but very promising results about a substance called ELEOTIN. ELEOTIN shows a few attributes that establish itself as a strong candidate for a long-term solution to diabetes and its complications. Let us repeat that the tests are quite preliminary. But the test results clearly indicate:
* ELEOTIN enhances insulin secretion from pancreatic ß-cells
* ELEOTIN upregulates insulin receptors leading to an increase in insulin binding
* ELEOTIN inhibits breakdown of complex carbohydrates into monosaccharides
* ELEOTIN increases the glucose transporter (GLUT2) expression in ß-cells
In addition, ELEOTIN does not have any known side effects, toxicity, and does not develop any resistance.