Insulin is a hormone that — in people without diabetes — ferries glucose, or blood sugar, to cells for energy or to be stored for later use. In people with diabetes, cells are resistant to insulin; as a result of this insulin resistance, sugar accumulates in the blood. While eating sugar by itself does not cause insulin resistance, Grieger says, foods with sugar and fat can contribute to weight gain, thereby reducing insulin sensitivity in the body.

Type 1 diabetes mellitus is characterized by loss of the insulin-producing beta cells of the pancreatic islets, leading to insulin deficiency. This type can be further classified as immune-mediated or idiopathic. The majority of type 1 diabetes is of the immune-mediated nature, in which a T cell-mediated autoimmune attack leads to the loss of beta cells and thus insulin.[38] It causes approximately 10% of diabetes mellitus cases in North America and Europe. Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Type 1 diabetes can affect children or adults, but was traditionally termed "juvenile diabetes" because a majority of these diabetes cases were found in children.[citation needed]


a broadly applied term used to denote a complex group of syndromes that have in common a disturbance in the oxidation and utilization of glucose, which is secondary to a malfunction of the beta cells of the pancreas, whose function is the production and release of insulin. Because insulin is involved in the metabolism of carbohydrates, proteins and fats, diabetes is not limited to a disturbance of glucose homeostasis alone.
To diagnose diabetes, doctors will  take a medical history (ask you about symptoms) and ask for blood and urine samples. Finding protein and sugar in the urine are signs of type 2 diabetes. Increased glucose and triglyceride (a type of lipid or fat) levels in the blood are also common findings. In most cases, blood glucose levels are checked after a person has been fasting for 8 hours.
The 1989 "St. Vincent Declaration"[117][118] was the result of international efforts to improve the care accorded to those with diabetes. Doing so is important not only in terms of quality of life and life expectancy but also economically – expenses due to diabetes have been shown to be a major drain on health – and productivity-related resources for healthcare systems and governments.
DM affects at least 16 million U.S. residents, ranks seventh as a cause of death in the United States, and costs the national economy over $100 billion yearly. The striking increase in the prevalence of DM in the U.S. during recent years has been linked to a rise in the prevalence of obesity. About 95% of those with DM have Type 2, in which the pancreatic beta cells retain some insulin-producing potential, and the rest have Type 1, in which exogenous insulin is required for long-term survival. In Type 1 DM, which typically causes symptoms before age 25, an autoimmune process is responsible for beta cell destruction. Type 2 DM is characterized by insulin resistance in peripheral tissues as well as a defect in insulin secretion by beta cells. Insulin regulates carbohydrate metabolism by mediating the rapid transport of glucose and amino acids from the circulation into muscle and other tissue cells, by promoting the storage of glucose in liver cells as glycogen, and by inhibiting gluconeogenesis. The normal stimulus for the release of insulin from the pancreas is a rise in the concentration of glucose in circulating blood, which typically occurs within a few minutes after a meal. When such a rise elicits an appropriate insulin response, so that the blood level of glucose falls again as it is taken into cells, glucose tolerance is said to be normal. The central fact in DM is an impairment of glucose tolerance of such a degree as to threaten or impair health. Long recognized as an independent risk factor for cardiovascular disease, DM is often associated with other risk factors, including disorders of lipid metabolism (elevation of very-low-density lipoprotein cholesterol and triglycerides and depression of high-density lipoprotein cholesterol), obesity, hypertension, and impairment of renal function. Sustained elevation of serum glucose and triglycerides aggravates the biochemical defect inherent in DM by impairing insulin secretion, insulin-mediated glucose uptake by cells, and hepatic regulation of glucose output. Long-term consequences of the diabetic state include macrovascular complications (premature or accelerated atherosclerosis with resulting coronary, cerebral, and peripheral vascular insufficiency) and microvascular complications (retinopathy, nephropathy, and neuropathy). It is estimated that half those with DM already have some complications when the diagnosis is made. The American Diabetes Association (ADA) recommends screening for DM for people with risk factors such as obesity, age 45 years or older, family history of DM, or history of gestational diabetes. If screening yields normal results, it should be repeated every 3 years. The diagnosis of DM depends on measurement of plasma glucose concentration. The diagnosis is confirmed when any two measurements of plasma glucose performed on different days yield levels at or above established thresholds: in the fasting state, 126 mg/dL (7 mmol/L); 2 hours postprandially (after a 75-g oral glucose load) or at random, 200 mg/dL (11.1 mmol/L). A fasting plasma glucose of 100-125 mg/dL (5.5-6.9 mmol/L) or a 2-hour postprandial glucose of 140-199 mg/dL (7.8-11 mmol/L) is defined as impaired glucose tolerance. People with impaired glucose tolerance are at higher risk of developing DM within 10 years. For such people, lifestyle modification such as weight reduction and exercise may prevent or postpone the onset of frank DM. Current recommendations for the management of DM emphasize education and individualization of therapy. Controlled studies have shown that rigorous maintenance of plasma glucose levels as near to normal as possible at all times substantially reduces the incidence and severity of long-term complications, particularly microvascular complications. Such control involves limitation of dietary carbohydrate and saturated fat; monitoring of blood glucose, including self-testing by the patient and periodic determination of glycosylated hemoglobin; and administration of insulin (particularly in Type 1 DM), drugs that stimulate endogenous insulin production (in Type 2 DM), or both. The ADA recommends inclusion of healthful carbohydrate-containing foods such as whole grains, fruits, vegetables, and low-fat milk in a diabetic diet. Restriction of dietary fat to less than 10% of total calories is recommended for people with diabetes, as for the general population. Further restriction may be appropriate for those with heart disease or elevated cholesterol or triglyceride levels. The ADA advises that high-protein, low-carbohydrate diets have no particular merit in long-term weight control or in maintenance of a normal plasma glucose level in DM. Pharmaceutical agents developed during the 1990s improve control of DM by enhancing responsiveness of cells to insulin, counteracting insulin resistance, and reducing postprandial carbohydrate absorption. Tailor-made insulin analogues produced by recombinant DNA technology (for example, lispro, aspart, and glargine insulins) have broadened the range of pharmacologic properties and treatment options available. Their use improves both short-term and long-term control of plasma glucose and is associated with fewer episodes of hypoglycemia. SEE ALSO insulin resistance

Diabetes mellitus (DM) is best defined as a syndrome characterized by inappropriate fasting or postprandial hyperglycemia, caused by absolute or relative insulin deficiency and its metabolic consequences, which include disturbed metabolism of protein and fat. This syndrome results from a combination of deficiency of insulin secretion and its action. Diabetes mellitus occurs when the normal constant of the product of insulin secretion times insulin sensitivity, a parabolic function termed the “disposition index” (Figure 19-1), is inadequate to prevent hyperglycemia and its clinical consequences of polyuria, polydipsia, and weight loss. At high degrees of insulin sensitivity, small declines in the ability to secrete insulin cause only mild, clinically imperceptible defects in glucose metabolism. However, irrespective of insulin sensitivity, a minimum amount of insulin is necessary for normal metabolism. Thus, near absolute deficiency of insulin must result in severe metabolic disturbance as occurs in type 1 diabetes mellitus (T1DM). By contrast, with decreasing sensitivity to its action, higher amounts of insulin secretion are required for a normal disposition index. At a critical point in the disposition index curve (see Figure 19-1), a further small decrement in insulin sensitivity requires a large increase in insulin secretion; those who can mount these higher rates of insulin secretion retain normal glucose metabolism, whereas those who cannot increase their insulin secretion because of genetic or acquired defects now manifest clinical diabetes as occurs in type 2 diabetes (T2DM).
At present, the American Diabetes Association does not recommend general screening of the population for type 1 diabetes, though screening of high risk individuals, such as those with a first degree relative (sibling or parent) with type 1 diabetes should be encouraged. Type 1 diabetes tends to occur in young, lean individuals, usually before 30 years of age; however, older patients do present with this form of diabetes on occasion. This subgroup is referred to as latent autoimmune diabetes in adults (LADA). LADA is a slow, progressive form of type 1 diabetes. Of all the people with diabetes, only approximately 10% have type 1 diabetes and the remaining 90% have type 2 diabetes.
Diabetes insipidus is considered very rare in less 20,000 cases diagnosed per year. Diabetes mellitus is more common, with type 2 diabetes being more common than type 1. There are more than 3 million cases of type 2 diabetes. Unlike diabetes mellitus, diabetes insipidus is not treated by controlling insulin levels. Depending on your symptoms, your doctor may prescribe a low-salt diet, hormone therapy, or have you increase your water intake. 
The tuberculosis skin test is based on the fact that infection with M. tuberculosis produces a delayed-type hypersensitivity skin reaction to certain components of the bacterium. The standard recommended tuberculin test is administered by injecting 0.1mL of 5 TU (tuberculin units) PPD into the top layers of skin of the forearm. "Reading" the skin test means detecting a raised, thickened local area of skin reaction, referred to as induration. The area of induration (palpable, raised, hardened area) around the site of injection is the reaction to tuberculin.
People usually develop type 2 diabetes after the age of 40 years, although people of South Asian origin are at an increased risk of the condition and may develop diabetes from the age of 25 onwards. The condition is also becoming increasingly common among children and adolescents across all populations. Type 2 diabetes often develops as a result of overweight, obesity and lack of physical activity and diabetes prevalence is on the rise worldwide as these problems become more widespread.

Most cases of diabetes involve many genes, with each being a small contributor to an increased probability of becoming a type 2 diabetic.[10] If one identical twin has diabetes, the chance of the other developing diabetes within his lifetime is greater than 90%, while the rate for nonidentical siblings is 25–50%.[13] As of 2011, more than 36 genes had been found that contribute to the risk of type 2 diabetes.[37] All of these genes together still only account for 10% of the total heritable component of the disease.[37] The TCF7L2 allele, for example, increases the risk of developing diabetes by 1.5 times and is the greatest risk of the common genetic variants.[13] Most of the genes linked to diabetes are involved in beta cell functions.[13]


There are many complications of diabetes. Knowing and understanding the signs of these complications is important. If caught early, some of these complications can be treated and prevented from getting worse. The best way to prevent complications of diabetes is to keep your blood sugars in good control. High glucose levels produce changes in the blood vessels themselves, as well as in blood cells (primarily erythrocytes) that impair blood flow to various organs.
What you need to know about borderline diabetes Borderline diabetes, known as prediabetes, is a condition where blood sugar levels are higher than normal but not yet high enough to be type 2 diabetes. This MNT Knowledge Center article explains the signs to look out for, how to monitor the disease, and ways to prevent it becoming full diabetes. Read now
Feeling famished all the time? Your body could be trying to tell you that something’s up with your blood sugar. Many people with diabetes experience extreme hunger when their condition is unmanaged, thanks to high blood sugar levels. When your body can’t effectively convert the sugar in your blood into usable energy, this may leave you pining for every sandwich or sweet you see. And if you’re looking for a filling snack that won’t put your health at risk, enjoy one of the 25 Best and Worst Low-Sugar Protein Bars!
The definition of a genetic disease is a disorder or condition caused by abnormalities in a person's genome. Some types of genetic inheritance include single inheritance, including cystic fibrosis, sickle cell anemia, Marfan syndrome, and hemochromatosis. Other types of genetic diseases include multifactorial inheritance. Still other types of genetic diseases include chromosome abnormalities (for example, Turner syndrome, and Klinefelter syndrome), and mitochondrial inheritance (for example, epilepsy and dementia).
When the glucose concentration in the blood remains high over time, the kidneys will reach a threshold of reabsorption, and glucose will be excreted in the urine (glycosuria).[62] This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume will be replaced osmotically from water held in body cells and other body compartments, causing dehydration and increased thirst (polydipsia).[60]
Diabetes mellitus (DM), commonly referred to as diabetes, is a group of metabolic disorders in which there are high blood sugar levels over a prolonged period.[10] Symptoms of high blood sugar include frequent urination, increased thirst, and increased hunger.[2] If left untreated, diabetes can cause many complications.[2] Acute complications can include diabetic ketoacidosis, hyperosmolar hyperglycemic state, or death.[3] Serious long-term complications include cardiovascular disease, stroke, chronic kidney disease, foot ulcers, and damage to the eyes.[2]
An article published in November 2012 in the journal Global Public Health found that countries with more access to HFCS tended to have higher rates of the disease. Though it’s likely that these countries’ overall eating habits play a role in their populations’ diabetes risk, a study published in February 2013 in the journal PLoS One found limiting access to HFCS in particular may help reduce rates of the diagnosis.
The classic symptoms of diabetes such as polyuria, polydypsia and polyphagia occur commonly in type 1 diabetes, which has a rapid development of severe hyperglycaemia and also in type 2 diabetes with very high levels of hyperglycaemia. Severe weight loss is common only in type 1 diabetes or if type 2 diabetes remains undetected for a long period. Unexplained weight loss, fatigue and restlessness and body pain are also common signs of undetected diabetes. Symptoms that are mild or have gradual development could also remain unnoticed.
Several common medications can impair the body's use of insulin, causing a condition known as secondary diabetes. These medications include treatments for high blood pressure (furosemide, clonidine, and thiazide diuretics), drugs with hormonal activity (oral contraceptives, thyroid hormone, progestins, and glucocorticorids), and the anti-inflammation drug indomethacin. Several drugs that are used to treat mood disorders (such as anxiety and depression) also can impair glucose absorption. These drugs include haloperidol, lithium carbonate, phenothiazines, tricyclic antidepressants, and adrenergic agonists. Other medications that can cause diabetes symptoms include isoniazid, nicotinic acid, cimetidine, and heparin. A 2004 study found that low levels of the essential mineral chromium in the body may be linked to increased risk for diseases associated with insulin resistance.
Although some people with this type of diabetes are thin, the majority of people (90%) are overweight. Losing weight, even 2 kg to 5 kg (5 lbs to 10 lbs) can help lower blood glucose levels. For many people, following a healthy diet and an exercise program may be all that is needed to help control glucose levels. For others, healthy eating and exercise alone aren't enough to lower blood glucose levels.

In type 2 diabetes, there also is a steady decline of beta cells that adds to the process of elevated blood sugars. Essentially, if someone is resistant to insulin, the body can, to some degree, increase production of insulin and overcome the level of resistance. After time, if production decreases and insulin cannot be released as vigorously, hyperglycemia develops.

People with T2D produce insulin, but their bodies don’t use it correctly; this is referred to as being insulin resistant. People with type 2 diabetes may also be unable to produce enough insulin to handle the glucose in their body. In these instances, insulin is needed to allow the glucose to travel from the bloodstream into our cells, where it’s used to create energy.
If you are symptomatic (e.g., increased thirst or urination, unexplained weight loss), your doctor may only use a single test to diagnose diabetes/prediabetes. If you don't have any symptoms, one high blood glucose test doesn't necessarily mean you have diabetes/prediabetes. Your doctor will repeat one of the blood tests again on another day (generally 1 week later) to confirm the diagnosis.
While many experts believe that most type 1 genes have been identified, the situation with type 2 diabetes is much different. A recent study found that the known genetic links to type 2 probably account for only about 6 percent of the genetic predisposition for that form of diabetes. This could mean either that some of the genes discovered have a bigger effect than is currently believed or that "we are still missing 94 percent of the genes," says Atul Butte, MD, PhD, an assistant professor of pediatrics at Stanford University.
Insulin resistance is the most common cause of type 2 diabetes, but it is possible to have type 2 and not be insulin resistant. You can have a form of type 2 where you body simply doesn’t produce enough insulin; that’s not as common. Researchers aren’t sure what exactly keeps some people from producing enough insulin, but that’s another thing they’re working hard to figure out.

The above tips are important for you. But it's also crucial to allow yourself time to cope with the diagnosis and commit to making lifestyle changes that will benefit you forever. The good news is the diabetes is a manageable disease; the tough part is that you must think about it daily. Consider finding support—someone that you can talk to about your struggles—be that a friend, another person with diabetes, or a loved one. This may seem trivial, but it truly can help you take control of diabetes so that it doesn't control you. Some next steps that may help you to get on the right track at this early stage in your journey:

Type 2 Diabetes: Accounting for 90 to 95 percent of those with diabetes, type 2 is the most common form. Usually, it's diagnosed in adults over age 40 and 80 percent of those with type 2 diabetes are overweight. Because of the increase in obesity, type 2 diabetes is being diagnosed at younger ages, including in children. Initially in type 2 diabetes, insulin is produced, but the insulin doesn't function properly, leading to a condition called insulin resistance. Eventually, most people with type 2 diabetes suffer from decreased insulin production.
The glucose level at which symptoms develop varies greatly from individual to individual (and from time to time in the same individual), depending in part on the duration of diabetes, the frequency of hypoglycemic episodes, the rate of fall of glycemia, and overall control. (Glucose is also the sole energy source for erythrocytes and the kidney medulla.)
People with type 1 diabetes are unable to produce any insulin at all. People with type 2 diabetes still produce insulin, however, the cells in the muscles, liver and fat tissue are inefficient at absorbing the insulin and cannot regulate glucose well. As a result, the body tries to compensate by having the pancreas pump out more insulin. But the pancreas slowly loses the ability to produce enough insulin, and as a result, the cells don’t get the energy they need to function properly.

Insulin is essential to process carbohydrates, fat, and protein. Insulin reduces blood glucose levels by allowing glucose to enter muscle cells and by stimulating the conversion of glucose to glycogen (glycogenesis) as a carbohydrate store. Insulin also inhibits the release of stored glucose from liver glycogen (glycogenolysis) and slows the breakdown of fat to triglycerides, free fatty acids, and ketones. It also stimulates fat storage. Additionally, insulin inhibits the breakdown of protein and fat for glucose production (gluconeogenesis) in the liver and kidneys.
Symptoms of type 1 diabetes can start quickly, in a matter of weeks. Symptoms of type 2 diabetes often develop slowly—over the course of several years—and can be so mild that you might not even notice them. Many people with type 2 diabetes have no symptoms. Some people do not find out they have the disease until they have diabetes-related health problems, such as blurred vision or heart trouble.

Regular ophthalmological examinations are recommended for early detection of diabetic retinopathy. The patient is educated about diabetes, its possible complications and their management, and the importance of adherence to the prescribed therapy. The patient is taught the importance of maintaining normal blood pressure levels (120/80 mm Hg or lower). Control of even mild-to-moderate hypertension results in fewer diabetic complications, esp. nephropathy, cerebrovascular disease, and cardiovascular disease. Limiting alcohol intake to approximately one drink daily and avoiding tobacco are also important for self-management. Emotional support and a realistic assessment of the patient's condition are offered; this assessment should stress that, with proper treatment, the patient can have a near-normal lifestyle and life expectancy. Long-term goals for a patient with diabetes should include achieving and maintaining optimal metabolic outcomes to prevent complications; modifying diet and lifestyle to prevent and treat obesity, dyslipidemia, cardiovascular disease, hypertension, and nephropathy; improving physical activity; and allowing for the patient’s nutritional and psychosocial needs and preferences. Assistance is offered to help the patient develop positive coping strategies. It is estimated that 23 million Americans will be diabetic by the year 2030. The increasing prevalence of obesity coincides with the increasing incidence of diabetes; approx. 45% of those diagnosed receive optimal care according to established guidelines. According to the CDC, the NIH, and the ADA, about 40% of Americans between ages 40 and 74 have prediabetes, putting them at increased risk for type 2 diabetes and cardiovascular disease. Lifestyle changes with a focus on decreasing obesity can prevent or delay the onset of diabetes in 58% of this population. The patient and family should be referred to local and national support and information groups and may require psychological counseling.
Insulin is a hormone produced by the beta cells within the pancreas in response to the intake of food. The role of insulin is to lower blood sugar (glucose) levels by allowing cells in the muscle, liver and fat to take up sugar from the bloodstream that has been absorbed from food, and store it away as energy. In type 1 diabetes (previously called insulin-dependent diabetes mellitus), the insulin-producing cells are destroyed and the body is not able to produce insulin naturally. This means that sugar is not stored away but is constantly released from energy stores giving rise to high sugar levels in the blood. This in turn causes dehydration and thirst (because the high glucose ‘spills over’ into the urine and pulls water out of the body at the same time). To exacerbate the problem, because the body is not making insulin it ‘thinks’ that it is starving so does everything it can to release even more stores of energy into the bloodstream. So, if left untreated, patients become increasingly unwell, lose weight, and develop a condition called diabetic ketoacidosis, which is due to the excessive release of acidic energy stores and causes severe changes to how energy is used and stored in the body.
Studies in type 1 patients have shown that in intensively treated patients, diabetic eye disease decreased by 76%, kidney disease decreased by 54%, and nerve disease decreased by 60%. More recently the EDIC trial has shown that type 1 diabetes is also associated with increased heart disease, similar to type 2 diabetes. However, the price for aggressive blood sugar control is a two to three fold increase in the incidence of abnormally low blood sugar levels (caused by the diabetes medications). For this reason, tight control of diabetes to achieve glucose levels between 70 to120 mg/dl is not recommended for children under 13 years of age, patients with severe recurrent hypoglycemia, patients unaware of their hypoglycemia, and patients with far advanced diabetes complications. To achieve optimal glucose control without an undue risk of abnormally lowering blood sugar levels, patients with type 1 diabetes must monitor their blood glucose at least four times a day and administer insulin at least three times per day. In patients with type 2 diabetes, aggressive blood sugar control has similar beneficial effects on the eyes, kidneys, nerves and blood vessels.
Insulin is released into the blood by beta cells (β-cells), found in the islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Lower glucose levels result in decreased insulin release from the beta cells and in the breakdown of glycogen to glucose. This process is mainly controlled by the hormone glucagon, which acts in the opposite manner to insulin.[61]

People with type 1 diabetes are unable to produce any insulin at all. People with type 2 diabetes still produce insulin, however, the cells in the muscles, liver and fat tissue are inefficient at absorbing the insulin and cannot regulate glucose well. As a result, the body tries to compensate by having the pancreas pump out more insulin. But the pancreas slowly loses the ability to produce enough insulin, and as a result, the cells don’t get the energy they need to function properly.


In this health topic, we explain the dangers of hyperglycemia, or high blood sugar levels, and diabetes. Hyperglycemia causes many of the warning signs of diabetes listed above. Hyperglycemia may be caused by skipping or forgetting your insulin or diabetes medicine, eating too many grams of carbs for the amount of insulin administered, simply eating too many grams of carbs in general, or from stress or infections.
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