Diabetes mellitus (IPA: / da bi ti z/ or / da bi t s/, /m la t s/ or / m l t s/), ), is a syndrome characterized often referred to simply as diabetes (Greek: by disordered metabolism and abnormally high

blood sugar (hyperglycaemia) resulting from insufficient levels of the hormoneinsulin.[2] The characteristic symptoms are excessive urine production (polyuria) due to high blood glucose levels, excessive thirst and increased fluid intake (polydipsia) attempting to compensate for increased urination, blurred vision due to high blood glucose effects on the eye's optics, unexplained weight loss, and lethargy. These symptoms are likely to be less apparent if the blood sugar is only mildly elevated. The World Health Organization recognizes three main forms of diabetes mellitus: type 1, type 2, andgestational diabetes (occurring during pregnancy),[3] which have different causes and population distributions. While, ultimately, all forms are due to the beta cells of the pancreas being unable to produce sufficient insulin to prevent hyperglycemia, the causes are different.[4] Type 1 diabetes is usually due to autoimmune destruction of the pancreatic beta cells. Type 2 diabetes is characterized by insulin resistance in target tissues. This causes a need for abnormally high amounts of insulin and diabetes develops when the beta cells cannot meet this demand. Gestational diabetes is similar to type 2 diabetes in that it involves insulin resistance; the hormones of pregnancy can cause insulin resistance in women genetically predisposed to developing this condition. Gestational diabetes typically resolves with delivery of the child, however types 1 and 2 diabetes arechronic conditions.[2] All types have been treatable since insulin became medically available in 1921. Type 1 diabetes, in which insulin is not secreted by the pancreas, is directly treatable only with injected insulin, although dietary and other lifestyle adjustments are part of management. Type 2 may be managed with a combination of dietary treatment, tablets and injections and, frequently, insulin supplementation. While insulin was originally produced from natural sources such as porcine pancreas, most insulin used today is produced through genetic engineering, either as a direct copy of human insulin, or human insulin with modified molecules that provide different onset and duration of action. Insulin can also be delivered continuously by a specialized pump which subcutaneously provides insulin through a changeable catheter. Diabetes can cause many complications. Acute complications (hypoglycemia, ketoacidosis, ornonketotic hyperosmolar coma) may occur if the disease is not adequately controlled. Serious long-term complications include cardiovascular disease (doubled risk), chronic renal failure, retinal damage (which can lead to blindness), nerve damage (of several kinds), and microvascular damage, which may cause impotence and poor healing. Poor healing

of wounds, particularly of the feet, can lead to gangrene, which may require amputation. Adequate treatment of diabetes, as well as increased emphasis on blood pressure control and lifestyle factors (such as not smoking and keeping a healthy body weight), may improve the risk profile of most aforementioned complications. In the developed world, diabetes is the most significant cause of adult blindness in the non-elderly and the leading cause of non-traumatic amputation in adults, and diabetic nephropathy is the main illness requiring renal dialysis in the United States.[5]

Classification
The term diabetes, without qualification, usually refers to diabetes mellitus, which is associated with excessive sweet urine (known as "glycosuria") but there are several rarer conditions also named diabetes. The most common of these is diabetes insipidus in which the urine is not sweet (insipidus meaning "without taste" in Latin); it can be caused by either kidney (nephrogenic DI) or pituitary gland(central DI) damage. The principal two idiopathic forms of diabetes mellitus are known as types 1 and 2. The term "type 1 diabetes" has universally replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes (IDDM). Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and non-insulin-dependent diabetes (NIDDM). Beyond these two types, there is no agreed-upon standard nomenclature. Various sources have defined "type 3 diabetes" as, among others, gestational diabetes,[6] insulin-resistant type 1 diabetes (or "double diabetes"), type 2 diabetes which has progressed to require injected insulin, and latent autoimmune diabetes of adults (or LADA or "type 1.5" diabetes.[7]) There is also maturity onset diabetes of the young (MODY) which is a group of several single gene disorders with strong family histories that present as type 2 diabetes before 30 years of age.

Type 1 diabetes mellitus
Main article: Diabetes mellitus type 1 Type 1 diabetes mellitus is characterized by loss of the insulin-producing beta cells of the islets of Langerhans in the pancreas, leading to a deficiency of insulin. The main cause of this beta cell loss is a Tcell mediated autoimmune attack.[4] There is no known preventive measure which can be taken against type 1 diabetes; it is about 10% of diabetes mellitus cases in North America and Europe (though this varies by geographical location), and is a higher percentage in some other areas. 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

is replacement of insulin combined with careful monitoring of blood glucose levels using blood testing monitors. As the disease . At this stage hyperglycemia can be reversed by a variety of measures and medications that improve insulin sensitivity or reduce glucose production by the liver. it is also possible to deliver insulin by a pump. In the early stage the predominant abnormality is reduced insulin sensitivity. low levels of blood glucose. An inhaled form of insulin. insulin is replaced in a non-physiological manner. although Pfizer discontinued the product for business reasons in October 2007. [8] Type 1 treatment must be continued indefinitely in essentially all cases. appropriate care. However. and this approach is therefore far from ideal. 4±6 mmol/l) as is safely possible. Treatment need not significantly impair normal activities. The average glucose level for the type 1 patient should be as close to normal (80± 120 mg/dl. However. The principal treatment of type 1 diabetes. Values above 300 mg/dl (15 mmol/l) usually require medical treatment and may lead to ketoacidosis. Type 2 diabetes mellitus Main article: Diabetes mellitus type 2 Type 2 diabetes mellitus is characterized differently due to insulin resistance or reduced insulin sensitivity. calledhypoglycemia. Values above 200 mg/dl (10 mmol/l) is sometimes accompanied by discomfort and frequent urination leading to dehydration. Exubera. treatment is burdensome for patients. and the ability to program doses (a bolus) of insulin as needed at meal times. Treatment emphasis is now also placed on lifestyle adjustments (diet and exercise) though these cannot reverse the progress of the disease. such as frequent hypoglycemic events. Some physicians suggest up to 140±150 mg/dl (7-7. Without insulin. although they are not immediately lifethreatening. even from its earliest stages. may lead to seizures or episodes of unconsciousness and absolutely must be treated immediately.5 mmol/l) for those having trouble with lower values. awareness."juvenile diabetes" because it represents a majority of the diabetes cases in children. The defective responsiveness of body tissues to insulin almost certainly involves the insulin receptor in cell membranes. was approved by the FDA in January 2006. combined with reduced insulin secretion. discipline in testing and dosing of insulin is taken. characterized by elevated levels of insulin in the blood. diabetic ketoacidosis often develops which may result in coma or death. Apart from the common subcutaneous injections. which allows continuous infusion of insulin 24 hours a day at preset levels. if sufficient patient training.

likely in connection with the increased prevalence of childhood obesity seen in recent decades in some places. loss of sensation or pain due to diabetic neuropathy. metformin). sulfonylureas).g. including renal failure due to diabetic nephropathy. It is sometimes possible to achieve long-term. thiazolidinediones).[11] Oral medication may eventually fail due to further . Type 2 diabetes is usually first treated by increasing physical activity.progresses the impairment of insulin secretion worsens.. and losing weight.[10] Type 2 diabetes may go unnoticed for years because visible symptoms are typically mild.. severe long-term complications can result from unnoticed type 2 diabetes. for example around 5 kg (10 to 15 lb). the underlying tendency to insulin resistance is not lost. Abdominal fat is especially active hormonally. Insulin production is initially only moderately impaired in type 2 diabetes. and so attention to diet. The usual next step. and liver damage from non-alcoholic steatohepatitis.g. and to substantially attenuate insulin resistance (e. most especially when it is in abdominal fat deposits.[9] Other factors include aging (about 20% of elderly patients in North America have diabetes) and family history (type 2 is much more common in those with close relatives who have had it). and weight loss must continue.g. so oral medication (often used in various combinations) can be used to improve insulin production (e. vision damage due to diabetic retinopathy. if necessary. and usually there are no ketoacidotic episodes. According to one study. However. 42% for diabetes related death and 36% for all cause mortality and stroke. Obesity is found in approximately 55% of patients diagnosed with type 2 diabetes.. exercise. There are numerous theories as to the exact cause and mechanism in type 2 diabetes. overweight patients treated with metformin compared with diet alone. secreting a group of hormones called adipokines that may possibly impair glucose tolerance. hadrelative risk reductions of 32% for any diabetes endpoint. but not subcutaneous fat) is known to predispose individuals for insulin resistance. vascular disease (including coronary artery disease). However. These can restore insulin sensitivity even when the weight loss is modest. decreasing carbohydrate intake. to regulate inappropriate release of glucose by the liver and attenuate insulin resistance to some extent (e. non-existent or sporadic. is treatment with oral antidiabetic drugs. Central obesity (fat concentrated around the waist in relation to abdominal organs. and therapeutic replacement of insulin often becomes necessary. type 2 diabetes has increasingly begun to affect children and adolescents. satisfactory glucose control with these measures alone. In the last decade.

Other types There are several rare causes of diabetes mellitus that do not fit into type 1. this form is . type 2. as well as increasing the potential that the children of diabetic mothers will also become diabetic in the future. which is what separates it from type 2 diabetes). Gestational diabetes is fully treatable but requires careful medical supervision throughout the pregnancy. congenital cardiac and central nervous system anomalies. Gestational diabetes Main article: Gestational diabetes Gestational diabetes mellitus (GDM) resembles type 2 diabetes in several respects. Hyperbilirubinemia may result from red blood cell destruction. Risks to the baby include macrosomia (high birth weight). Even though it may be transient. or gestational diabetes. [12] This is particularly problematic as diabetes raises the risk of complications during pregnancy. At this point. A 2008 study completed in the U. insulin therapy is necessary to maintain normal or near normal glucose levels. such as shoulder dystocia. perinatal death may occur. untreated gestational diabetes can damage the health of the fetus or mother. In severe cases. A cesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia.impairment of beta cell insulin secretion. About 20%±50% of affected women develop type 2 diabetes later in life. found that more American women are entering pregnancy with preexisting diabetes. Induction may be indicated with decreased placental function.S. Increased fetal insulin may inhibit fetal surfactant production and cause respiratory distress syndrome. most commonly as a result of poor placental profusion due to vascular impairment. attempts to classify them remain controversial. Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal. It occurs in about 2%±5% of all pregnancies and may improve or disappear after delivery. In fact the rate of diabetes in expectant mothers has more than doubled in the past 6 years. and skeletal muscle malformations. involving a combination of relatively inadequate insulin secretion and responsiveness.

causing dehydration and increased thirst.[3] Signs and symptoms The classical triad of diabetes symptoms is polyuria. polydipsia and polyphagia. Symptoms may develop quite rapidly (weeks or months) in type 1 diabetes. resulting in increased urine production (polyuria) and increased fluid loss. When the glucose concentration in the blood is raised beyond the renal threshold. Abnormal insulin action may also have been genetically determined in some cases. ICD-10 code E12). which leads to changes in the shape of the lenses of the eyes. was deprecated by the World Health Organization when the current taxonomy was introduced in 1999. frequent urination. The ICD-10 (1992) diagnostic entity. which are. chronic pancreatitis and cystic fibrosis). Genetic mutations (autosomal ormitochondrial) can lead to defects in beta cell function. but should still be suspected. Blurred vision is a common complaint leading to a diabetes diagnosis. .very uncommon. particularly in children. and part of the glucose remains in the urine(glycosuria). However. in type 2 diabetes the symptoms develop much more slowly and may be subtle or completely absent. and increased appetite. Lost blood volume will be replaced osmotically from water held in body cells. respectively. Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). type 1 should always be suspected in cases of rapid vision change whereas type 2 is generally more gradual. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example. increased thirst and consequent increased fluid intake. All of these symptoms except weight loss can also manifest in type 2 diabetes in patients whose diabetes is poorly controlled. Type 1 diabetes may also cause a rapid yet significant weight loss (despite normal or even increased eating) and irreducible fatigue. Prolonged high blood glucose causes glucose absorption. reabsorption of glucose in the proximal renal tubuli is incomplete. This increases the osmotic pressure of the urine and inhibits the reabsorption of water by the kidney. malnutrition-related diabetes mellitus(MRDM or MMDM. resulting in vision changes. Many drugs impair insulin secretion and some toxins damage pancreatic beta cells.

Patients (usually with type 1 diabetes) may also present with diabetic ketoacidosis (DKA). There is a genetic element in individual susceptibility to some of these triggers which has been traced to particular HLA genotypes (i. or in a less common group.. Type 1 diabetes appears to be triggered by some (mainly viral) infections. coma may follow. a rapid. by stress or environmental exposure (such as exposure to certain chemicals or drugs).Concordance among monozygotic twins is close to 100%. even in those who have inherited the susceptibility. deep breathing known as Kussmaul breathing. the patient has been drinking extreme amounts of sugar-containing drinks. and any of many altered states of consciousness or arousal (such as hostility and mania or. There is a stronger inheritance pattern for type 2 diabetes. Genetics Both type 1 and type 2 diabetes are at least partly inherited. A small proportion of people with type 1 diabetes carry a mutated gene that causes maturity onset diabetes of the young (MODY). Candidate genes include KCNJ11 (potassium inwardly rectifying channel. Often. A rarer but equally severe possibility is hyperosmolar nonketotic state. which encodes the islet ATPsensitive potassium channel Kir6. Diabetic ketoacidosis is a medical emergency and requires hospital admission. Those with first-degree relatives with type 2 have a much higher risk of developing type 2. leading to a vicious circle in regard to the water loss. member 11). which regulates proglucagon gene expression and thus the production of glucagon-like peptide-1. vomiting and abdominal pain.[4] Moreover. confusion and lethargy). In severe DKA. progressing to death. increasing with the number of those relatives. equally. and about 25% of those with the disease have a family history of diabetes. which is more common in type 2 diabetes and is mainly the result of dehydration due to loss of body water. the genetic "self" identifiers relied upon by the immune system). type 1 diabetes mellitus seems to require an environmental trigger. nausea. polyuria.2.[13] .e. and TCF7L2 (transcription factor 7±like 2). obesity (which is an independent risk factor for type 2 diabetes) is strongly inherited. However. subfamily J. an extreme state of metabolic dysregulation characterized by the smell of acetone on the patient's breath.

optic atrophy. via exocytosis. found in the Islets of Langerhans in the pancreas. Insulin is released into the blood by beta cells ( -cells). diabetes mellitus. which is primarily triggered by food. hence the acronym DIDMOAD. Therefore deficiency of insulin or the insensitivity of itsreceptors plays a central role in all forms of diabetes mellitus. chiefly food containing absorbable glucose. It consists of diabetes insipidus.[14] Pathophysiology Mechanism of insulin release in normal pancreatic beta cells. in response to rising levels of blood glucose after eating. and deafness.Various hereditary conditions may feature diabetes. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel. the principal carbohydrate found in blood and used by the body as fuel. for conversion to other needed molecules. or for . It is stored within vacuoles pending release. Insulin production is more or less constant within the beta cells. but not central nervous system cells). Wolfram's syndrome is an autosomal recessive neurodegenerative disorder that first becomes evident in childhood. for example myotonic dystrophy and Friedreich's ataxia. irrespective of blood glucose levels. Much of the carbohydrate in food is converted within a few hours to themonosaccharideglucose. The chief trigger is a rise in blood glucose levels after eating Insulin is the principal hormone that regulates uptake of glucose from the blood into most cells (primarily muscle and fat cells.

such as a heart attack. certain eye problems.storage. muscle cells lack the necessary export mechanism. often accompanied by weight loss. Insulin (or its lack) is the principal signal in converting many of the bidirectional processes of metabolism from a catabolic to an anabolic direction. and fat storage. Diagnosis The diagnosis of type 1 diabetes. protein synthesis. Glucose thus recovered by the liver re-enters the bloodstream. poor wound healing or a foot ulcer. detection of hyperglycemia during other medical investigations. poor protein synthesis. If the amount of insulin available is insufficient. Diabetes mellitus is characterized by recurrent or persistent . certain fungal infections. about a quarter of people with new type 1 diabetes have developed some degree of diabetic ketoacidosis by the time the diabetes is recognized. and many cases of type 2. then glucose will not be absorbed properly by those body cells that require it nor will it be stored appropriately in the liver and muscles. Lowered glucose levels result both in the reduced release of insulin from the beta cells and in the reverse conversion of glycogen to glucose when glucose levels fall. The net effect is persistent high levels of blood glucose. or if the insulin itself is defective. This is mainly controlled by the hormone glucagon which acts in an opposite manner to insulin. These include ordinary health screening. The diagnosis of other types of diabetes is usually made in other ways. Insulin is also the principal control signal for conversion of glucose to glycogen for internal storage in liver and muscle cells. stroke. a low insulin level is the trigger for entering or leaving ketosis (the fat burning metabolic phase). and secondary symptoms such as vision changes or unexplainable fatigue. or delivering a baby with macrosomia or hypoglycemia. In particular. Diabetes is often detected when a person suffers a problem that is frequently caused by diabetes. is usually prompted by recent-onset symptoms of excessive urination (polyuria) and excessive thirst (polydipsia).neuropathy. such as acidosis. and other metabolic derangements. These symptoms typically worsen over days to weeks. if cells respond poorly to the effects of insulin (insulin insensitivity or resistance). Higher insulin levels increase some anabolic ("building up") processes such as cell growth and duplication. and vice versa.

y y Patients with fasting glucose levels between 110 and 125 mg/dL (6. and may be a random blood glucose test. Patients with plasma glucose at or above 140 mg/dL or 7. The current recommended goal for HbA1c in patients with diabetes is <7. However. a fasting blood glucose test.1 mmol/l).0% or higher (the 2003 revised U.hyperglycemia. an elevated level of glucose irreversibly bound to hemoglobin (termedglycosylated hemoglobin or HbA1c) of 6. A positive result. standard) is considered abnormal by most labs. HbA1c is primarily used as a treatment-tracking test reflecting average blood glucose levels over the preceding 90 days (approximately). should be confirmed by another of the above-listed methods on a different day. The screening test varies according to circumstances and local policy. in the absence of clinical symptoms of diabetes.1 and 7. including retinopathy and diabetic nephropathy. plasma glucose at or above 200 mg/dL (11.S.0 mmol/l) are considered to have impaired fasting glycemia. Of these two pre-diabetic states.0%. the latter in particular is a major risk factor for progression to full-blown diabetes mellitus as well as cardiovascular disease. Most physicians prefer to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing.0 mmol/l) is considered diagnostic for diabetes mellitus.8 mmol/l two hours after a 75 g oral glucose load are considered to have impaired glucose tolerance. a blood . although some guidelines are stricter (<6. According to the current definition. People with diabetes who have HbA1c levels within this range have a significantly lower incidence of complications from diabetes. which takes two hours to complete. and is diagnosed by demonstrating any one of the following:[3] fasting plasma glucose level at or above 126 mg/dL (7. which is considered good glycemic control. some physicians may order this test at the time of diagnosis to track changes over time. y random plasma glucose at or above 200 mg/dL (11. While not used for diagnosis.1 mmol/l) two hours after a 75 g oral glucose load as in a glucose tolerance test. and for those with any of several risk factors.[15][16] Screening Diabetes screening is recommended for many people at various stages of life.0 mmol/l). two fasting glucose measurements above 126 mg/dL (7.5%).

some chemotherapy agents (especially Lasparaginase).[17][18] Many medical conditions are associated with diabetes and warrant screening. including high-dose glucocorticoids. fatty liver. several mitochondrial neuropathies and myopathies. but no firm evidence has been found. or an even more formal glucose tolerance test.polycystic ovary syndrome. The risk of diabetes is higher with chronic use of several medications. past gestational diabetes. as well as some of the antipsychotics and mood stabilizers (especiallyphenothiazines and some atypical antipsychotics). screening for diabetic retinopathy has helped reduce the incidence of legal blindness since its implementation. and an uncontrolled autoimmune response that attacks the insulin producing beta cells. though the causal relationship is obscure. chronic pancreatitis. Many healthcare providers recommend universal screening for adults at age 40 or 50. cystic fibrosis. myotonic dystrophy.[23] . some of the inherited forms of neonatal hyperinsulinism. hemochromatosis. Native American. coronary artery disease. A partial list includes: high blood pressure.[19] Some research has suggested that breastfeedingdecreased the risk in later life. family history of diabetes. and often periodically thereafter. Earlier screening is typically recommended for those with risk factors such as obesity. elevated cholesterol levels. an unknown environmental trigger (suspected to be an infection. Friedreich's ataxia. and South Asian ancestry). Afro-Caribbean. [22] Giving children 2000 IU of Vitamin D during their first year of life is associated with reduced risk of type 1 diabetes.[citation needed] Prevention Type 1 diabetes risk is known to depend upon a genetic predisposition based on HLA types (particularly types DR3 and DR4). In the UK. [20][21] various other nutritional risk factors are being studied. Pacific Island. This includes yearly urine testing for microalbuminuria and examination of the retina (retinal photography) for retinopathy. highrisk ethnicity (Hispanic. People with a confirmed diagnosis of diabetes are screened routinely for complications.glucose test two hours after 75 g of glucose. although none has proven definitive in all cases).

but who received no vitamin B3. self glucose monitoring. There is inadequate evidence that eating foods of low glycemic index is clinically helpful despite recommendations and suggested diets in favor. at early stages of an immune reaction to them) but no overt diabetes. but it is interesting to note that moderate alcohol intake may reduce the risk (though heavy consumption absolutely clearly increases damage to body systems significantly).[24] Type 2 diabetes risk can be reduced in many cases by making changes in diet and increasing physical activity. having a modest fat intake.[26] rosiglitazone. without a cure. with the goal of keeping both short-term blood glucose levels.[27] There are numerous studies which suggest connections with some aspect of Type II diabetes with ingestion of certain foods or with some drugs. sensible exercise. and medical emphasis must necessarily be on managing/avoiding possible short-term as well as long-term diabetes-related problems.[28] orvalsartan.[31] Treatment and management Main article: Diabetes management Diabetes mellitus is currently a chronic disease. incidence of diabetes was reduced by 77% though causal mechanisms are unclear. had less than half the diabetes onset incidence in a 7-year time span as did the general population. and long term levels as well. within acceptable bounds.[30] Breastfeeding may also be associated with the prevention of type 2 of the disease in mothers.Children with antibodies to beta cell proteins (ie. Careful control is needed to reduce the risk of long term . There is an exceptionally important role for patient education.[25][26] The American Diabetes Association (ADA) recommends maintaining a healthy weight. getting at least 2½ hours of exercise per week (several brisk sustained walks appears sufficient). dietetic support. and treated with vitamin B-3 (niacin). and an even lower incidence relative to those with antibodies as above. and eating a good amount of fiber and whole grains. The ADA does not recommend alcohol consumption as a preventive.[29] In patients on hydroxychloroquine for rheumatoid arthritis. Some studies have shown delayed progression to diabetes in predisposed patients through prophylactic use of metformin.

g. the United States in the developed world). physioth erapists. difficult blood sugar control.complications. and Omnipod. the combination of Lantus/Levemir and Humalog. Optometrists. and if necessary. or nurse practitioners may jointly provide multidisciplinary expertise. Certified Diabetes Educators and DSNs (Diabetic Specialist Nurse)). given the associated higher risks of cardiovascular disease. wearingdiabetic socks. various oral diabetic drugs (type 2 only). In countries where patients must provide their own health care (i. lifestyle modifications should be undertaken to control blood pressure[32]and cholesterol by exercising more. Animas. In other circumstances.. patients are often advised to receive regular consultation from a physician (e. exercise and weight loss (type 2). such as the United Kingdom. the failure of the islets of Langerhans) has led to the study of several possible schemes to cure this form of diabetes mostly . at least every three to six months). care may take place mainly outside hospitals. or research projects. podiatrists/chiropodists. In countries using a general practitioner system. The fact that type 1 diabetes is due to the failure of one of the cell types of a single organ with a relatively simple function (i. Novolog or Apidra.e. general practitioners and specialists share care of a patient in a team approach. taking any of several drugs to reduce pressure. Medtronic Minimed. Many Type 1 treatments include the combination use of regular or NPH insulin. with hospital-based specialist care used only in case of complications. This is theoretically achievable with combinations of diet. the impact of out-ofpocket costs of diabetic care can be high. Another Type 1 treatment option is the use of the insulin pump with some of the most popular pump brands being: Cozmo. and insulin use (type 1 and increasingly for type 2 not responding to oral medications). consuming an appropriate diet..e.dietitians. Novolog or Apidra. and/or synthetic insulin analogs such as Humalog. In addition to the medications and supplies needed. In addition. smoking cessation. clinical nurse specialists (eg. Cure Cures for type 1 diabetes Main article: Cure for diabetes mellitus type 1 There is no practical cure now for type 1 diabetes.

[34] Still. showing similar or improved survival rates over a kidney transplant alone.by replacing the pancreas or just the beta cells. but this measure is not yet practical in regular clinical practice partly due to the limited number of beta cell donors. nephropathy) and become insulinindependent may now be considered "cured" from their diabetes.[35] An alternative technique has been proposed to place transplanted beta cells in a semi-permeable container. it has been shown that a type of gastric bypass surgery can normalize blood . it has provoked an immune reaction and long-term immunosuppressive drugs have been needed to protect the transplanted tissue. A simultaneous pancreas-kidney transplant is a promising solution. Stem cell research has also been suggested as a potential avenue for a cure since it may permit regrowth of Islet cells which are genetically part of the treated individual. But. like any such transplant. isolating and protecting them from the immune system.[33] Only those type 1 diabetics who have received either a pancreas or a kidney-pancreas transplant (often when they have developed diabetic kidney disease (ie. they generally remain on long-termimmunosuppressive drugs and there is a possibility that the immune system will mount a host versus graft response against the transplanted organ. and a 2007 trial of 15 newly diagnosed patients with type 1 diabetes treated withstem cells raised from their own bone marrow after immune suppression showed that the majority did not require any insulin treatment for prolonged periods of time. closed-loop insulin pumps. Cures for type 2 diabetes Type 2 has had no cure. in some sense. These are. At least two approaches have been demonstrated in vitro.[33] Transplants of exogenous beta cells have been performed experimentally in both mice and humans. thus perhaps eliminating the need for immunosuppressants.[36] Microscopic or nanotechnological approaches are under investigation as well. Thus far.[33] This has been done in mice. very recently. in one proposed case with implanted stores of insulin metered out by a rapid response valve sensitive to blood glucose levels.

[42][43] Wider health problems accelerate the deleterious effects of diabetes.[38] This surgery has been widely performed on morbidly obese patients and has had the additional the benefit of reducing the death rate from all causes by up to 40%. This approach may become a standard treatment for some people with type 2 diabetes in the near future. its removal eliminates the source of an unknown hormone that contributes to insulin resistance. [37] One hypothesis is that the proximal small intestine is dysfunctional in type 2 diabetes. and lack of regular exercise. understanding. elevated cholesterol levels. The precise causal mechanisms are being intensively researched.glucose levels in 80-100% of severely obese patients.[39] A small number of normal to moderately obese patients with type 2 diabetes have successfully undergone similar operations. to avoid hypoglycemia or other complications). The pattern of secretion of gastrointestinal hormones is changed by the bypass and removal of the duodenum and proximal jejunum. which together form the upper (proximal) part of thesmall intestine. The effect is not due to weight loss because it usually occurs within days of surgery. high blood pressure. . few people actually seem to go into total 'remission. However patients should talk to their doctors about this for real expectations before undertaking it (esp. and eat healthy diets may be able to keep some of the disease or some of the effects of the disease in 'remission. lose weight. and participation is vital since the complications of diabetes are far less common and less severe in people who have well-controlled blood sugar levels. These include smoking.[40][41] Prognosis Patient education. According to a study. Anecdotal evidence suggests that some of those with type 2 diabetes who exercise regularly. women with high blood pressure have a threefold risk of developing diabetes.' but some may find they need less of their insulin medications since the body tends to have lower insulin requirements during and shortly following exercise. obesity.' Certainly these tips can help prevent people predisposed to type 2 diabetes and those at pre-diabetic stages from actually developing the disorder as it helps restore insulin sensitivity. which is before significant weight loss happens.

Lack of insulin causes the liver to turn fat into ketone bodies for use as fuel. and breathing rapidly and deeply. proper treatment usually results in full recovery. and take into account health status. Abdominal pain is common and may be severe.[44] Agerelated glucose intolerance in humans is often accompanied by insulin resistance. Additionally. [45] Treatment goals for older patients with diabetes vary with the individual. hypoglycemia . and willingness to adhere to a treatment regimen. and death. though death can result from inadequate or delayed treatment. the patient in DKA is typically dehydrated. On presentation at hospital. and the decreased tissue sensitivity to insulin. Urine analysis reveals significant levels of ketone bodies (which spill over from the blood when the kidneys filter blood) well before overt symptoms. Insulin production decreases because of age-related impairment of pancreatic beta cells. Prompt. particularly intra-abdominal fat. as well as life expectancy. insulin resistance increases because of the loss of lean tissue and the accumulation of fat. leading to a high prevalence of type 2 diabetes and postchallenge hyperglycemia in the older population. shock. but circulating insulin levels are similar to those of younger people. there are certainly other benefits to this healthy lifestyle for both diabetics and nondiabetics. but can become a serious problem if sustained. level of dependence. DKA is always a medical emergency and requires medical . leading to DKA. Nevertheless. The level of consciousness is typically normal until late in the process.[46] Acute complications Main articles: Diabetic ketoacidosis . Glucose tolerance progressively declines with age. Elevated levels of ketone bodies in the blood decrease the blood's pH. nonketotic hyperosmolar coma . This is normal when periodic. anddiabetic coma Diabetic ketoacidosis Diabetic ketoacidosis (DKA) is an acute and dangerous complication that is always a medical emergency. Ketoacidosis can become severe enough to cause hypotension. The way diabetes is managed changes with age. or from complications.Regardless of whether it works that way or not for an individual. when lethargy may progress to coma.

In insulin- . Consciousness can be altered or even lost in extreme cases. If fluid is not replaced (by mouth or intravenously). Lethargy may ultimately progress to a coma. such as too much or incorrectly timed insulin. especially volume replacement. increments in epinephrine are the primary glucose counterregulatory factors that normally prevent or rapidly correct hypoglycemia. the osmotic effect of high glucose levels combined with the loss of water will eventually lead to dehydration. absent the latter. is an acute complication of several diabetes treatments. In patients with diabetes. leading to coma. Nonketotic hyperosmolar coma Hyperosmolar nonketotic state (HNS) is an acute complication sharing many symptoms with DKA.attention. Decrements in insulin. urgent medical treatment is necessary. sweaty. The patient may become agitated. water is drawn out of cells into the blood byosmosis and the kidneys dump glucose into the urine. seizures. The body's cells become progressively dehydrated as water is taken from them and excreted. As with DKA. It is more accurate to note that iatrogenic hypoglycemia is typically the result of the interplay of absolute (or relative) insulin excess and compromised glucose counterregulation in type 1 and advanced type 2 diabetes. but an entirely different cause and different treatment. but this is an over-simplification. or abnormally low blood glucose. or even brain damage and death. This results in loss of water and an increase in blood osmolarity. increments in glucagon. Electrolyte imbalances are also common and dangerous. In a person with very high blood glucose levels (usually considered to be above 300 mg/dl (16 mmol/l)). which is more common in type 2 diabetes than type 1. this may be caused by several factors. Hypoglycemia Hypoglycemia. Ketoacidosis is much more common in type 1 diabetes than type 2. and have many symptoms of sympatheticactivation of the autonomic nervous system resulting in feelings similar to dread and immobilized panic. too much or incorrectly timed exercise (exercise decreases insulin requirements) or not enough food (specifically glucose-producing carbohydrates). and.

They then form more surface glycoproteins than normal. In many cases (but not all). an injection ofglucagon (a hormone with the opposite effects of insulin) or an intravenous infusion of dextrose is used for treatment. Chronic complications Vascular disease Chronic elevation of blood glucose level leads to damage of blood vessels (angiopathy). hypoglycemia is treated with sugary drinks or food. and cause the basement membrane to grow thicker and weaker. In most cases. . Furthermore. and the combination of deficient glucagon and epinephrine responses causes defective glucose counterregulation. antecedent hypoglycemia leads to a vicious cycle of recurrent hypoglycemia and further impairment of glucose counterregulation. since they don't depend on insulin. Theendothelial cells lining the blood vessels take in more glucose than normal. intravenous dextrose is often used. In severe cases.deficient diabetes (exogenous) insulin levels do not decrease as glucose levels fall. The concept of hypoglycemia-associated autonomic failure (HAAF) in diabetes posits that recent incidents of hypoglycemia causes both defective glucose counterregulation and hypoglycemia unawareness. short-term avoidance of hypoglycemia reverses hypoglycemia unawareness in most affected patients. In hospitals. In diabetes. reduced sympathoadrenal responses can cause hypoglycemia unawareness. the resulting problems are grouped under "microvascular disease" (due to damage to small blood vessels) and "macrovascular disease" (due to damage to the arteries). By shifting glycemic thresholds for the sympathoadrenal (including epinephrine) and the resulting neurogenic responses to lower plasma glucose concentrations. although this is easier in theory than it is in practice. but usually only if the person is unconscious.

Macrovascular disease leads to cardiovascular disease. which contributes to intermittent claudication (exertion-related leg and foot pain) as well as diabetic foot. which can cause one or more of the following: Diabetic retinopathy. abnormal and decreased sensation. damage to the kidney which can lead to chronic renal failure. y Diabetic neuropathy. Retinal damage (from microangiopathy) makes it the most common cause of blindness among non-elderly adults in the US. leading to angina or myocardial infarction ("heart attack") Stroke (mainly the ischemic type) Peripheral vascular disease. damage to the heart. Other forms of diabetic neuropathy may present as mononeuritis or autonomic neuropathy. later often fingers and hands.Image of fundus showing scatter laser surgery fordiabetic retinopathy The damage to small blood vessels leads to amicroangiopathy. to which accelerated atherosclerosis is a contributor: y y y y Coronary artery disease. usually in a 'glove and stocking' distribution starting with the feet but potentially in other nerves. y Diabetic nephropathy. eventually requiring dialysis. y Diabetic cardiomyopathy. Diabetes mellitus is the most common cause of adult kidney failure worldwide in the developed world. which can lead to severe vision loss or blindness. When combined with damaged blood vessels this can lead to diabetic foot (see below). Diabetic amyotrophyis muscle weakness due to neuropathy. leading to diastolic dysfunction and eventuallyheart failure. growth of friable and poor-quality new blood vessels in the retina as well as macular edema(swelling of the macula). .

however.Diabetic myonecrosis ('muscle wasting') Diabetic foot. some of it most compellingly presented. It is the most common cause of adult amputation. perhaps most importantly a "Westernstyle" diet. including alterations to the vascular supply of the brain and the interaction of insulin with the brain itself.e.8% of the population. y Carotid artery stenosis does not occur more often in diabetes. diabetes does cause higher morbidity. in the developed world. This has suggested an environmental (i. in serious cases. Various mechanisms are proposed.[49] However. expected to occur in Asia and Africa. However. but there is little understanding of the mechanism(s) at present. but is more common (especially type 2) in the more developed countries. It is why diabetics are prone to leg and foot infections and why it takes longer for them to heal from leg and foot wounds. at least 171 million people worldwide suffer from diabetes. and there appears to be a lower prevalence of abdominal aortic aneurysm. and it is estimated that by the year 2030. according to the World Health Organization.[49] Its incidence is increasing rapidly. may cause skin ulcer andinfection and. Epidemiology In 2000.[48]. the criteria for diagnosing diabetes in the USA mean that it is more readily diagnosed than in .. dietary) effect. though there is much speculation. where most patients will likely be found by 2030.[47] Diabetic encephalopathy is the increased cognitive decline and risk of dementia observed in diabetes. necrosis and gangrene. or 2. mortality and operative risks with these conditions. usually of toes and or feet.[49] Diabetes mellitus occurs throughout the world. this number will almost double. often due to a combination of neuropathy and arterial disease.[49] The increase in incidence of diabetes in developing countries follows the trend of urbanization and lifestyle changes. The greatest increase in prevalence is.

The American Diabetes Association point out the 2003 assessment of the National Center for Chronic Disease Prevention and Health Promotion (Centers for Disease Control and Prevention) that 1 in 3 Americans born after 2000 will develop diabetes in their lifetime. Most of this difference is not currently understood. 18% to 20% have diabetes. most prominently type 2. The Centers for Disease Control has termed the change an epidemic.[51][52] According to the American Diabetes Association.[50] TheNational Diabetes Information Clearinghouse estimates that diabetes costs $132 billion in the United States alone every year. [53] Diabetes mellitus prevalence increases with age.6 million) of Americans age 60 and older have diabetes. The National Health and Nutrition Examination Survey (NHANES III) demonstrated that. In Australia the age-standardised prevalence of self-reported diabetes in Indigenous Australians is almost 4 times that of non-indigenous Australians. . About 5%±10% of diabetes cases in North America are type 1. in the population over 65 years old.[44] Indigenous populations in first world countries have a higher prevalence and increasing incidence of diabetes than their corresponding non-indigenous populations. this is likely due to both differences in the rate of type 1 and differences in the rate of other types.[54] Preventative community health programs such as Sugar Man (diabetes education) are showing some success in tackling this problem.some other countries. The fraction of type 1 in other parts of the world differs. with the rest being type 2. and the numbers of older persons with diabetes are expected to grow as the elderly population increases in number. approximately 18. with 40% having either diabetes or its precursor form of impaired glucose tolerance.3% (8.