Diabetes mellitus is a condition in which the amount of glucose (sugar) in the bloodstream is too high because the body cannot use it properly. Glucose is used as fuel or as building bloc and comes from digested carbohydrates in food (bread, rice, potatoes) or from the liver where it is stored (in a special form as glycogen). It is important to keep the concentration of glucose at strict levels, since excess blood sugar levels cause vision problems, kidney damage, nerve damage, heart and circulation problems.

The World Health Organization now recognizes three main forms of diabetes mellitus: type 1, type 2, and gestational diabetes (occurring during pregnancy), which have different causes and population distributions. Gestational diabetes typically resolves with delivery of the child, however types 1 and 2 diabetes are chronic conditions.

In diabetic patients glucose is not well transported into the body cells because either the level of the helper hormone insulin is too low (type-1) or the body cells do not respond to it properly (type-2). In response to the high blood sugar levels, kidneys work double time to get rid of it. Because of the frequent urination, people with diabetes crave for more liquid to maintain a proper water level in the body.

The full name "diabetes mellitus" is a combination of a Greek and a Latin word. Aretaeus the Cappadocian, a physician living in Alexandria during the second century, chose the Greek word "diabetes" (passing through) to describe a patient exhibiting excessive urination. Mellis is a Latin word meaning honey. Mellitus therefore refers to the sweet taste of the urine of diabetes patients.

Diabetes is one of the oldest known human diseases. Ancient Persians, Indians, and Egyptians have described the symptoms, but it is only since a hundred years that we have developed a proper understanding of the condition. A number of researchers in the beginning of the 20th century have contributed to the notion that extracts from the pancreas had positive effects when tested on diabetic dogs.

In 1921 Eli Lilly (now a global pharmaceutical company) was able to produce large quantities of highly refined animal-sourced extracts that showed no ill side effects. The insulin preparations, named after the pancreatic islet cells, were commercialised shortly thereafter. It was subsequently discovered that the hormone insulin is needed to allow glucose to pass from the bloodstream into the body cells where it is used as fuel or as building bloc.

The pancreas, from which the extracts were made, is located close to the stomach. Much of the pancreas consists of cells that secrete digestive enzymes - a special type of proteins - into the gastrointestinal tract. The digestive enzymes catalyse the breakdown of large molecules in the food into smaller building blocks. One of these enzymes is a-amylase, that splits starch into small segments of multiple sugars and into the individual soluble sugars, mainly glucose.

Islets of Langerhans are special groups of cells in the pancreas. There are five types of cells in an islet: beta cells, which make insulin; alpha cells, which make glucagon; delta cells, which make somatostaton; and PP cells and D1 cells, about which little is known.

For thousands of years, contraction of diabetes meant wasting away to a certain death. While much progress has been made, as described below, diabetes is ranked among the leading causes of blindness, renal failure and lower limb amputation. Cardiovascular disease is among 70-80% of people with diabetes the leading cause of death. The huge socio-economic costs through human suffering, disability and premature mortality are very relevant complications when seen in a public health perspective.

Evidence of tissue damage can be found in many organ systems such as the kidneys, eyes, peripheral nerves and vascular system. It is not fully understood how diabetes leads to this complex array of complications. However, it is certain that the toxic effects of high glucose levels, along with the impact of elevated blood pressure, abnormal lipid levels and both functional and structural abnormalities of small blood vessels are involved.

The first medical scientists that undertook definite steps to try and treat diabetics were dr. Frederick Banting and his assistant Charles Best with the help of prof. J.J.R. MacLeod and prof. J.B. Collip, working at university laboratories in Toronto and Alberta, Canada in 1921. The researchers were able to produce pancreatic extracts which had anti diabetic characteristics when tested on diabetic dogs.

The first tests with the 14-year old diabetes patient Leonard Thompson, early in 1922, were a spectacular success. Despite his rigid diet of only 450 calories (the only known treatment at this time), Thompson continued to lose large amounts of glucose, while weighing only 65 pounds and he was about to slip into a coma and die. The injections of purified pancreatic extract caused his blood sugar to return to normal and gradually he lost the common symptoms of a diabetes patient.

The news about this success spread around the world quickly and gave immediate hope to terminally ill diabetic persons. Requests for the insulin preparations and its methodology of preparation followed. After treatment there were many patients in a diabetic coma that made miraculous recoveries. The first patient, Leonard Thompson, lived another 13 years using the first generation of insulin preparations. He died at the age of 27 due to diabetes complications, probably because of the difficulties of maintaining glucose concentrations at sufficiently steady levels and the less advanced therapeutic methods.

Insulin is not a cure, it can only help in alleviating the effects of the disease. However, its identification, isolation and the medical discoveries on its use continues to save millions of lives world-wide. The production of insulin has changed a great deal since 1922. Starting with crude non-human pancreatic extracts, modern science and technology has now made high quality recombinant insulin and technological advanced delivery systems available to diabetic persons.

The human body maintains the concentration of glucose in the bloodstream in the narrow of 0.7 gram and 1.1 gram per liter. If higher concentrations of glucose are measured, one is diagnosed with diabetes. Even after a meal or a sugar containing drink the level should not rise above 1.7 gram/L.

How does the body accomplish that? Glucagon and insulin are secreted from the Isle of Langerhans Alpha and Beta cells in the pancreas in response to low and high concentrations of blood glucose respectively. The pancreatic endocrine hormone glucagon is able to free glucose from glucagen, that is stored in the liver, while insulin instead stimulates white fat cells to take up glucose. The picture on the left shows the inverse relationship that both insulin and glucagon have to each other. The pancreas holds a central role in the production of these hormones and this ultimately may thus determine whether a patient has problems maintaining a good sugar balance.

While it became obvious that diabetes leads to a variety of complications if not treated well, it is not yet fully elucidated what the exact cellular or molecular events are behind the observed problems with vision, kidney damage, nerve damage, the heart and circulation. However it is certain that hyperglycemia (increased levels of blood glucose) is the principal cause of diabetes complications.

A suggested consequence of increased glucose concentrations is the increased rate at which so called advanced glycation end products (AGE) are created. AGEs are a range of different of molecules that are formed by a chemical reaction of reducing sugars with free amino groups of proteins, lipids, and nucleic acids. It is the same reaction that can be seen in the browning of fruit. In and around human cells the reaction turns functional molecules into useless cross-linked products.

It is normal that AGEs accumulate at a slow rate in the human body, thereby contributing to the process of ageing. But in diabetic patients, it is the increased rate at which AGEs are formed that poses a major problem. Driven by excess glucose, the reaction essentially speeds up the ageing process of important organs such as the kidney and a poor kidney function has devastating effects on health, particularly on the heart. AGEs are also found in the blood vessels of the retina and their increased levels in diabetic patients correlate with the enhanced occurrence of eye disease. AGE-crosslink formation results in arterial stiffening with loss of elasticity of large vessels, also termed atherosclerosis. Because of this, diabetic patients stand a significant greater risk cardiovascular and cerebrovascular mortality.

There is considerable interest in anti-glycation compounds because of their therapeutic potential. One candidate is aminoguanidine, an inhibitor of AGE formation, since it was shown to prevent retinopathy (eye disease) in diabetic animals. Carnosine (beta-alanyl-L-histidine), and aspirin may also inhibit the formation of the harmful AGE cross-links.

Other drugs that may disrupt already formed AGEs are also under active investigation. These compounds have the ability to remove the bound sugar and thus reverse the detrimental effects of advanced glycation. Alagebrium is such an AGE-breaker, but unfortunately, the promising results in animals were not sufficiently well replicated in human studies.

Prevention of the described problems is another option and this can be reached by two routes: by controlling bloodstream glucose concentrations and by reducing the intake of AGEs with food. AGEs are not only formed inside the body, they are also created during cooking. AGEs are typically formed when sugars are cooked with proteins or fats in the absence of water. Browning reactions during baking of meat or French fries are clear examples of glycation, although these create tasteful flavors. Food manufacturers even boost the flavor of natural foods by incorporating synthetic AGEs into foods. Consequently, the AGEs content of the Western diet has increased vastly in the past 50 years, as has the quantity of food consumed.

Studies have shown that eating a low-AGE diet can reduce levels of inflammation and chronic diseases. Smart things to do are to use "wet" cooking methods, such as boiling, steaming, stewing, and braising and to avoid pasteurized or dark fried and grilled foods.

As early as 1894, Schaefer suggested that islet tissue in the pancreas might be responsible for an internal secretion with effects on the blood sugar level. The name for the hormone insulin was separately suggested by Meyer in 1909 and Schaefer in 1913 and is derived from the Latin term insula, meaning island. The name thus correctly refers to the source of production of the hormone in the pancreatic islands of Langerhans.

Insulin is a small protein that is composed of two peptide chains of 21 and 30 amino acids each. The two chains are chemically interlinked at two positions. Insulin is produced in the Beta cells of the islets of Langerhans in the pancreas mostly in response to food intake and increased blood glucose levels.

Initially insulin could only be purified from animal sources in order to treat diabetics. The first successful insulin preparations came from cows that were slaughtered for food. Later, pancreatic tissues from pigs were also used for the isolation of insulin preparations, that enjoyed increasing purity. Even today bovine and porcine derived insulin would work very well for most diabetes patients. Bovine insulin differs from human insulin in only three amino acid residues, and porcine insulin in just one. Still some people may develop an adverse reaction to these non-human proteins.

The next step was taken by the advances in molecular genetic techniques. The amino acid sequence of bovine insulin was the absolute first protein to be completely determined by Sanger in 1955 and the first genetically-engineered copy of human insulin was produced in E. coli bacteria in 1977 at Genentech's laboratoria. The human genes which code for the two insulin protein chains A and B were chemically synthesised and then introduced into the DNA of these bacteria. Each chain was purified from the fermentation fluid of the two bacterial strains and then combined in a chemical step to form the exact copy of the human insulin molecule. The US Food and Drug Administration granted a marketing license in 1981. The pharmaceutical company Eli Lilly went on in 1982 to sell the first commercially available biosynthetic human insulin under the brand name Humulin.

Insulin, that is released in the bloodstream, causes most of the body's cells to take up glucose from the blood where it is either metabolized (used) or stored as glycogen (a branched chain of coupled glucose molecules). A fine tuned mechanism, involving insulin production and degradation, makes sure that the glucose levels in the blood remain at relative constant levels.

After insulin is released into the blood stream, it may bind to cells at specific protein sites called receptors. The insulin receptor protein serves to signal the inside of the cells that insulin is present at the outside. The receptor consists of two alpha subunits and two beta subunits. The alpha subunits occupy the outer surface of the cell, whereas the beta subunits span the cell membrane and also face cell interior. Only after the binding of insulin at the outer side, the interior part of this receptor protein can be modified by a specific enzymatic reaction (phosphorylation by tyrosine kinase). This process may then trigger the various actions on glucose metabolism in the particular cell, one of which is glucose uptake.

Glucose concentrations in the bloodstream rise (hyperglycemia) if insulin is low or absent (type-1 diabetes) or when glucose is not taken up by the body cells (type-2 diabetes). This condition is typical for diabetic patients and results in a range of symptoms: excessive thirst, excessive urination, poor wound healing. Recurrent high glucose levels cause damage to the blood vessels and to the organs they supply, leading to further complications of diabetes.

Too low concentrations of glucose in the bloodstream (hypoglycemia) can occur when insulin is administered but no food is taken. Glucose concentrations drop and while body cells may revert to the use fat as an energy source. Nervous cells only have very small internal stores of glycogen and therefore cannot cope well with hypoglycemia. Lack of sufficient glucose concentrations in the bloodstream can then cause the central nervous system to malfunction: dizziness and even loss of consciousness, known as "hypoglycemic coma" can occur. Severe acute or prolonged hypoglycemia may result in brain damage or death.

Type 1 diabetes is a chronic and non curable disease . Once you have it, you have it forever. Also, there is no known measure that one could take to prevent contracting type 1 diabetes. Most people that become affected by type 1 diabetes are otherwise healthy and of a healthy weight. Diet and exercise cannot reverse or prevent type 1 diabetes.

Type 1 diabetes is formerly known as insulin-dependent diabetes, childhood diabetes or juvenile diabetes. The exact cause(s) of contracting this type of diabetes is not yet established. Experts theorize that a viral infection may be the trigger of an autoimmune reaction that results in the destruction of the beta cells of the islets of Langerhans in the pancreas. Thus, by an unfortunate chain of events, the body's own defense system attacks the insulin producing cells, leading to absolute dependence on insulin treatment. Other hypotheses have also been postulated where environmental or genetic factors may play a role in the observed self destruction of the beta-cells. Another mystery is that Finland, Sardinia and Sweden have the highest incidence rates for type 1 diabetes in the world.

The onset of the disease typically occurs at a relatively young ages and generally not later than the age of 40. It is estimated that 5-10% of patients who are diagnosed with diabetes have type 1 diabetes. Type 1 diabetes may go unnoticed at first, since these are the symptoms:

Early diagnosis is important for someone who is at high risk for type 1 diabetes. Typically symptoms are weight loss within a short period of time, constant thirst and frequent urination. A (regular) check of blood glucose levels is the right action to take, in order to prevent possible organ damage that diabetes may bring about. Chronic elevation of blood glucose, even when no symptoms are present to alert the individual to the presence of diabetes, will eventually lead to tissue damage, with consequent, and often serious, disease.

Indeed, diabetes is often only diagnosed when other problems arise, that are caused by diabetes such as heart attack, stroke, eye problems, neuropathy, poor wound healing or a foot ulcer and certain fungal infections. Type 1 diabetes is lethal unless it is treated by insulin injections, replacing the missing hormone from the non-functional pancreas.

In most cases of type 1 diabetes, people have inherited risk factors from both parents that enhanced the chance of contracting the disease. It is a polygenic disease, meaning many different genes contribute to the risk of getting it. However apparently environmental factors can also influence this predisposition in a positive or possibly negative way. It was shown that if one twin of identical twins had type-1, the other would be affected in only 30-50% of these cases. Therefore in some cases, despite having the exact same genome, one twin had the disease, where the other did not. This shows that genetically at-risk individuals may respond differently to environmental factors. In some cases, the immune system will respond in a benign fashion, while in other cases it will begin an inflammatory response that can ultimately lead to diabetes.

One environmental trigger might be related to cold weather since type 1 diabetes develops more often in winter and is more common in places with cold climates. Certain virus infection have also been mentioned as non-genetic trigger to develop type 1 diabetes. A third factor might be a longer period of breastfeeding which may have a preventive role in the development of type-1 diabetes.

Diabetes type 1 treatment must be continued indefinitely with careful monitoring of blood glucose levels and subcutaneous insulin injections. However, treatment does not impair normal activities, if sufficient emphasis is placed on lifestyle adjustments (awareness, discipline in testing, medication, diet and exercise). The major goal in treating diabetes is to minimize any elevation of blood sugar (glucose) without causing abnormally low levels of blood sugar.

Instead of manual injections, insulin may also be administered, depending on the severity of the disease, as an inhaled powder, or by a pump, which allows intelligent infusion of insulin 24 hours a day at optimal levels.

The average glucose level in the bloodstream should be as close to normal (approximately 1 gram/Liter) as possible. If patients have frequent problems with too fast dropping glucose levels when insulin is administered, slightly higher values up to 1.5 gr./L. may be advised. Hyperglycemia occurs when values raise above 2 gr./L. which are considered too high. Levels above 3gr./L. require immediate treatment to prevent ketoacidosis.

If the blood glucose reaches such levels and the body cells are unable to use this glucose, stored fat will be used as an alternate energy source. When fat is burned for energy at high rates, ketones will be produced and get into the bloodstream. As the ketone levels rise, the blood becomes more and more acidic resulting in a range of life threatening effects. As soon as a person begins to vomit or has difficulty breathing, immediate treatment in an emergency room is required to prevent coma and possible death. On the other end of the scale, low levels of blood glucose, called hypoglycemia, may lead to seizures or episodes of unconsciousness.

Insulin injections and eating thus have to be harmonized with each other to prevent too high or deep level of glucose. Insulin became medically available in 1921 when it was produced from natural sources such as porcine pancreas. Today most insulin is produced through genetic engineering as a direct copy or a modified form of human insulin.

Organ transplants may be considered as an advanced treatment of type-1 diabetes. Often this is only an option in the case of kidney failure when a pancreas transplant can be done in conjunction with a kidney transplant. The side effects of a pancreas transplant can be significant, so pancreas transplant is typically reserved for those who have serious diabetes complications.

Another treatment that is less invasive is islet cell transplantation. In this case, islet cells are injected into the liver, where they should thrive and start producing insulin. In a study in the year 2000 pancreatic islet cells were transplanted into selected patients with type 1 diabetes that was difficult to control. In 2005 it turned out that 10 percent of the 65 patients who received transplants had remained free of the need for insulin injections. Most recipients returned to using insulin because the transplanted islets lost their ability to function over time. The researchers noted, however, that many transplant recipients were able to reduce their need for insulin and achieve better glucose stability.

Type 2 diabetes is the most common of the two main types and accounts for between 85 - 95% of all people with diabetes in developed countries. It is alarming that the incidence of type-2 diabetes is increasing rapidly, probably because larger sections of the world population adhere to western diet patterns. About 124 million people worldwide had diabetes by 1997, but in 2010 this number is estimated to reach 221 million.

People develop type 2 diabetes when the body can still make insulin, but the cells in the muscles, liver and fat do not respond to insulin properly - a condition known as insulin resistance. At first, the pancreas keeps up with the added demand by producing more insulin. In time, however, it loses the ability to secrete enough insulin in response to meals. Type 2 diabetes mellitus is formerly known as non­insulin-dependent diabetes since, when the disease develops initially, the administration of insulin is not yet needed.

In the early stage of type 2 diabetes the predominant abnormality is reduced insulin sensitivity, characterized by elevated levels of insulin in the blood. Beta cells produce increased amounts of insulin in response to elevated levels of glucose in the bloodstream, since the body cells have lost sensitivity towards insulin and do not take up the available glucose. This means that the level of glucose in the body remains higher for longer periods of time, as the cells that normally take in the glucose ignore the signals coming from the pancreas. In response to the enhanced levels of glucose, the beta cells in the pancreas put out more and more insulin. The body cells subsequently will also ignore the higher levels of insulin, resulting in a progressive escalation of the regulatory system.

Eventually, the beta cells wear out and cannot produce sufficient insulin anymore. Since muscle and fat cells cannot take up glucose without some amount of insulin, the patient must begin to inject themselves with insulin.

At an early stage hyperglycemia can be reversed by a variety of measures and medications that improve insulin sensitivity or reduce glucose production by the liver. In contrast to type-1 diabetes, persons with type 2 diabetes are not dependent on exogenous insulin and are not prone to ketosis, which means that minimal amounts of glucose at least reach the cells. Nevertheless type-2 patients may require insulin to control hyperglycaemia if this is not achieved with diet alone or with oral hypoglycaemic agents. As the disease is not treated properly and thus progresses the impairment of insulin secretion worsens, and therapeutic replacement of insulin may become necessary.

If type-2 diabetes is left untreated, the condition worsens and other problems, that are typical for type-1 diabetes, arise as well. Enhanced levels of glucose in the bloodstream permanently cause damage to organs and other parts of the body. When the walls of the arteries throughout the body are damaged, atherosclerosis occurs, which causes heart attacks and strokes. In the case of damage to small arteries, blood circulation decreases causing nerve damage and loss of sensation. Therefore small wounds go unnoticed while their healing is also diminished due to the decreased blood flow. If subsequently infection occurs that is left untreated with due care, foot or leg amputations are often the only way to treat the patient. Other failures that apply have already been described for type-1 diabetes.

Abdominal obesity, hypertension, elevated cholesterol levels and heart disease are common in most Western societies. Since these problems often go hand in hand with a sedentary lifestyle and non-balanced food habits, the condition is also described as 'metabolic syndrome'. Over 90% of patients that are diagnosed with type-2 diabetes are obese, therefore it was suggested that the coexistence of these diseases is not a coincidence, but that a common underlying abnormality allows them to develop. The question is what are the causes and which conditions are the results of the foregoing.

Type 2 diabetes therefore usually develops in people over the age of 40. However, recently, more children are being diagnosed with the condition, some as young as seven, probably because of unhealthy diets and spending too much time in front of television or computer. Type 2 diabetes can be easy to ignore, especially in the early stages when you're feeling fine. But the condition causes two main problems: i) body cells are starved for energy and ii) over time, high blood glucose levels may hurt body tissues in eyes, kidneys, nerves or heart.

The precise way in which insulin resistance develops is unclear, although genetics, diet and level of physical activity are believed to play prominent roles. Excessive intake of all carbohydrates, especially the sweet types, is a known risk factor in the development of insulin resistance. There is also a strong family correlation, but this could either mean that there may be genetic components involved, or it could mean that an 'inherited' lifestyle is the culprit. Therefore, a cause-and-effect relationship between insulin resistance, the coexisting conditions and the mechanisms through which insulin resistance influences their development or the other way around, has yet to be conclusively demonstrated.

Genetic factors play an important role in type 2 diabetes, but the pattern is complicated, since both impairment of beta cell function and an abnormal response to insulin are involved. Researchers have identified a number of genetic suspects.

There is also a theory that suggests that some cases of type 2 diabetes and obesity are derived from normal genetic actions that were once important for survival. Some experts postulate the existence of a so-called "thrifty" gene, which regulates hormonal fluctuations to accommodate seasonal changes. In certain nomadic populations, hormones are released during seasons when food supplies have traditionally been low, which results in resistance to insulin and efficient fat storage. The process is reversed in seasons when food is readily available. Because modern industrialization has made high-carbohydrate and fatty foods available all year long, the gene no longer serves a useful function and is now harmful because fat, originally stored for famine situations, is not used up. Such a theory could help explain the high incidence of type 2 diabetes and obesity found in Pima tribes and other Native American tribes with nomadic histories and newly introduced Western dietary habits.

Finding out you have diabetes is scary and type 2 diabetes is serious, but people with diabetes can live long, healthy, happy lives. Treatment for type 2 diabetes requires a lifelong commitment to monitor blood sugar levels, healthy eating, regular exercise and possibly, diabetes medication or insulin therapy. These steps will help keep blood sugar level closer to normal, which can delay or prevent complications.

The first steps to take in treating type-2 diabetes is weight reduction, exercise and the use of a diabetic diet. When these measures fail to control the elevated blood sugars, oral medications are used. If oral medications are still insufficient, treatment with insulin is considered.

Insulin resistance itself can be managed in two ways: i) the need for insulin can be reduced, and ii) the sensitivity of the body cells to insulin can be increased.

These treatments of existing type-2 diabetes have also shown to be useful in the prevention of the disease. Studies that were performed in Finland and in the US, showed that the described changes in diet and exercise reduced the development of diabetes by more than 50%.

However, if these treatments do not lower blood glucose concentrations sufficiently well, medication can be used in addition to the necessary change in life style. There are two types of drugs that are used to treat diabetes: those that lower blood sugar and raise insulin, and those that lower blood sugar and lower insulin also. The latter drugs must be tried first when trying to increase the sensitivity of the body cells to insulin.

One example is Metformin (Glucophage), which is the most popular oral anti-type-2 diabetic medicine used. In 2008 more than 40 million prescriptions were filled for the drug in the US. Metformin has two mechanisms of action that help to control blood glucose levels. It prevents the liver from releasing glucose into the blood, and it increases the sensitivity of muscle and fat cells to insulin so that they remove more glucose from the blood. Because of these actions, metformin reduces both glucose and insulin levels in the bloodstream. Metformin is a reasonably safe medication although there are gastrointestinal side effects in some people.

Gestational diabetes is a type of diabetes that starts during pregnancy. Pregnant women who have never had diabetes before but who have high blood sugar levels during pregnancy are said to have gestational diabetes. Gestational diabetes affects about 1%-5% of all pregnant women, depending on the populations measured. It may develop as early as the 20th week of pregnancy but generally the condition improves and disappears after the baby is born.

High sugar levels can be unhealthy for both the mother and the baby, therefore it is necessary to follow a diet, take exercise and have frequent blood tests to check the blood sugar level. It may be necessary to take a medicine to control the blood sugar level. Gestational diabetes also involves a combination of inadequate insulin secretion and responsiveness, resembling type-2 diabetes in several respects and about 20% - 50% of women with gestational diabetes develop type 2 diabetes later in life.

There are several rare causes of diabetes mellitus that do not fit into type 1, type 2, or gestational diabetes:

Diabetes prevalence:

Metabolic syndrome is defined as the presence of any three of the following conditions:

The ComScience project is a Cooperation Action (#230470) funded by the European Commission under the Seventh Framework Programme: FP7 - Capacities - Science in Society ComScience © 2009-12

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