Type 1 diabetes occurs because the insulin-producing cells of the pancreas (beta cells) are damaged. In type 1 diabetes, the pancreas makes little or no insulin, so sugar cannot get into the body's cells for use as energy. People with type 1 diabetes must use insulin injections to control their blood glucose. Type 1 is the most common form of diabetes in people who are under age 30, but it can occur at any age. Ten percent of people with diabetes are diagnosed with type 1.
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
Although age of onset and length of the disease process are related to the frequency with which vascular, renal, and neurologic complications develop, there are some patients who remain relatively free of sequelae even into the later years of their lives. Because diabetes mellitus is not a single disease but rather a complex constellation of syndromes, each patient has a unique response to the disease process.
Although age of onset and length of the disease process are related to the frequency with which vascular, renal, and neurologic complications develop, there are some patients who remain relatively free of sequelae even into the later years of their lives. Because diabetes mellitus is not a single disease but rather a complex constellation of syndromes, each patient has a unique response to the disease process.
Treatment involves drinking sufficient fluids to prevent dehydration.[1] Other treatments depend on the type.[1] In central and gestational DI, treatment is with desmopressin.[1] Nephrogenic DI may be treated by addressing the underlying cause or the use of a thiazide, aspirin or ibuprofen.[1] The number of new cases of diabetes insipidus each year is 3 in 100,000.[4] Central DI usually starts between the ages of 10 and 20 and occurs in males and females equally.[2] Nephrogenic DI can begin at any age.[3] The term "diabetes" is derived from the Greek word meaning siphon.[5]
Central diabetes insipidus. A synthetic, or man-made, hormone called desmopressin treats central diabetes insipidus. The medication comes as an injection, a nasal spray, or a pill. The medication works by replacing the vasopressin that a patient’s body normally produces. This treatment helps a patient manage symptoms of central diabetes insipidus; however, it does not cure the disease.
^ Emadian A, Andrews RC, England CY, Wallace V, Thompson JL (November 2015). "The effect of macronutrients on glycaemic control: a systematic review of dietary randomised controlled trials in overweight and obese adults with type 2 diabetes in which there was no difference in weight loss between treatment groups". The British Journal of Nutrition. 114 (10): 1656–66. doi:10.1017/S0007114515003475. PMC 4657029. PMID 26411958.

There are four types of DI, each with a different set of causes.[1] Central DI (CDI) is due to a lack of the hormone vasopressin (antidiuretic hormone).[1] This can be due to injury to the hypothalamus or pituitary gland or genetics.[1] Nephrogenic DI (NDI) occurs when the kidneys do not respond properly to vasopressin.[1] Dipsogenic DI is a result of excessive fluid intake due to damage to the hypothalamic thirst mechanism.[1] It occurs more often in those with certain psychiatric disorders or on certain medications.[1] Gestational DI occurs only during pregnancy.[1] Diagnosis is often based on urine tests, blood tests and the fluid deprivation test.[1] Diabetes mellitus is a separate condition with an unrelated mechanism, though both can result in the production of large amounts of urine.[1]
The primary treatment for diabetes insipidus involves drinking enough liquid to prevent dehydration. A health care provider may refer a person with diabetes insipidus to a nephrologist—a doctor who specializes in treating kidney problems—or to an endocrinologist—a doctor who specializes in treating disorders of the hormone-producing glands. Treatment for frequent urination or constant thirst depends on the patient’s type of diabetes insipidus:

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.
Your management plan will likely include a combination of nutritional guidelines, an exercise regimen, and medications designed to keep your blood sugar levels in check. They may also suggest regular blood sugar testing. It may take some trial and error to settle on a treatment plan that works the best for you. Be sure to talk to your healthcare team about any questions or concerns that you may have.
Type 1 diabetes can occur at any age, and a significant proportion is diagnosed during adulthood. Latent autoimmune diabetes of adults (LADA) is the diagnostic term applied when type 1 diabetes develops in adults; it has a slower onset than the same condition in children. Given this difference, some use the unofficial term "type 1.5 diabetes" for this condition. Adults with LADA are frequently initially misdiagnosed as having type 2 diabetes, based on age rather than cause[46]
Metformin is generally recommended as a first line treatment for type 2 diabetes, as there is good evidence that it decreases mortality.[7] It works by decreasing the liver's production of glucose.[90] Several other groups of drugs, mostly given by mouth, may also decrease blood sugar in type II DM. These include agents that increase insulin release, agents that decrease absorption of sugar from the intestines, agents that make the body more sensitive to insulin, and agents that increase the excretion of glucose in the urine.[90] When insulin is used in type 2 diabetes, a long-acting formulation is usually added initially, while continuing oral medications.[7] Doses of insulin are then increased to effect.[7][91]
central diabetes insipidus a metabolic disorder due to injury of the neurohypophyseal system, which results in a deficient quantity of antidiuretic hormone (ADH or vasopressin) being released or produced, resulting in failure of tubular reabsorption of water in the kidney. As a consequence, there is the passage of a large amount of urine having a low specific gravity, and great thirst; it is often attended by voracious appetite, loss of strength, and emaciation. Diabetes insipidus may be acquired through infection, neoplasm, trauma, or radiation injuries to the posterior lobe of the pituitary gland or it may be inherited or idiopathic.
2. Home glucose monitoring using either a visually read test or a digital readout of the glucose concentration in a drop of blood. Patients can usually learn to use the necessary equipment and perform finger sticks. They keep a daily record of findings and are taught to adjust insulin dosage accordingly. More recent glucose monitoring devices can draw blood from other locations on the body, such as the forearm.
FASTING GLUCOSE TEST. Blood is drawn from a vein in the patient's arm after a period at least eight hours when the patient has not eaten, usually in the morning before breakfast. The red blood cells are separated from the sample and the amount of glucose is measured in the remaining plasma. A plasma level of 7.8 mmol/L (200 mg/L) or greater can indicate diabetes. The fasting glucose test is usually repeated on another day to confirm the results.
The word "diabetes" (/ˌdaɪ.əˈbiːtiːz/ or /ˌdaɪ.əˈbiːtɪs/) comes from Latin diabētēs, which in turn comes from Ancient Greek διαβήτης (diabētēs) which literally means "a passer through; a siphon".[17] Ancient Greek physician Aretaeus of Cappadocia (fl. in the first century CE) used that word, with the intended meaning "excessive discharge of urine", as the name for the disease.[18][19] Ultimately, the word comes from Greek διαβαίνειν (diabainein), meaning "to pass through",[17] which is composed of δια- (dia-), meaning "through" and βαίνειν (bainein), meaning "to go".[18] The word "diabetes" is first recorded in English, in the form "diabete", in a medical text written around 1425.
The word "diabetes" (/ˌdaɪ.əˈbiːtiːz/ or /ˌdaɪ.əˈbiːtɪs/) comes from Latin diabētēs, which in turn comes from Ancient Greek διαβήτης (diabētēs) which literally means "a passer through; a siphon".[17] Ancient Greek physician Aretaeus of Cappadocia (fl. in the first century CE) used that word, with the intended meaning "excessive discharge of urine", as the name for the disease.[18][19] Ultimately, the word comes from Greek διαβαίνειν (diabainein), meaning "to pass through",[17] which is composed of δια- (dia-), meaning "through" and βαίνειν (bainein), meaning "to go".[18] The word "diabetes" is first recorded in English, in the form "diabete", in a medical text written around 1425.
Your body uses a system of organs and hormone signals to regulate body fluids. The kidneys play an important role in this fluid regulation by removing extra fluid from your bloodstream. The bladder stores this fluid waste until you urinate it out. Your body regulates fluid levels by making less urine when you need to replace fluid lost to sweating, or by making more urine when there is too much fluid in your body.
If the amount of insulin available is insufficient, or if cells respond poorly to the effects of insulin (insulin insensitivity or insulin resistance), or if the insulin itself is defective, then glucose is not absorbed properly by the body cells that require it, and is not stored appropriately in the liver and muscles. The net effect is persistently high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as acidosis.[62]
A chronic metabolic disorder marked by hyperglycemia. DM results either from failure of the pancreas to produce insulin (type 1 DM) or from insulin resistance, with inadequate insulin secretion to sustain normal metabolism (type 2 DM). Either type of DM may damage blood vessels, nerves, kidneys, the retina, and the developing fetus and the placenta during pregnancy. Type 1 or insulin-dependent DM has a prevalence of just 0.3 to 0.4%. Type 2 DM (formerly called adult-onset DM) has a prevalence in the general population of 6.6%. In some populations (such as older persons, Native Americans, African Americans, Pacific Islanders, Mexican Americans), it is present in nearly 20% of adults. Type 2 DM primarily affects obese middle-aged people with sedentary lifestyles, whereas type 1 DM usually occurs in children, most of whom are active and thin, although extremely obese children are now being diagnosed with type 2 diabetes as well. See: table; dawn phenomenon; insulin; insulin pump; insulin resistance; diabetic polyneuropathy; Somogyi phenomenon

Your doctor may use one or more tests to screen for diabetes. The glycated hemoglobin (A1C) test is most common. This is a blood test that indicates your average blood sugar level during the previous two to three months. It measures the amount of blood sugar attached to hemoglobin. The higher your blood sugar levels are, the more hemoglobin is attached to sugar.


Insulin Therapy. Exogenous insulin is given to patients with diabetes mellitus as a supplement to the insufficient amount of endogenous insulin that they produce. In some cases, this must make up for an absolute lack of insulin from the pancreas. Exogenous insulin is available in various types. It must be given by injection, usually subcutaneously, and because it is a potent drug, the dosage must be measured meticulously. Commonly, regular insulin, which is a fast-acting insulin with a short span of action, is mixed with one of the longer-acting insulins and both types are administered in one injection.
In nephrogenic DI, treating the cause may cure the problem. Other treatments include taking high doses of desmopressin, along with other drugs like diuretics, either alone or with aspirin or ibuprofen, or other types of this medication class such as indomethacin (TIVORBEX). When taking these medications, it’s important to drink water only when you’re thirsty.
People who are obese -- more than 20% over their ideal body weight for their height -- are at particularly high risk of developing type 2 diabetes and its related medical problems. Obese people have insulin resistance. With insulin resistance, the pancreas has to work overly hard to produce more insulin. But even then, there is not enough insulin to keep sugars normal.

^ Jump up to: a b Petzold A, Solimena M, Knoch KP (October 2015). "Mechanisms of Beta Cell Dysfunction Associated With Viral Infection". Current Diabetes Reports (Review). 15 (10): 73. doi:10.1007/s11892-015-0654-x. PMC 4539350. PMID 26280364. So far, none of the hypotheses accounting for virus-induced beta cell autoimmunity has been supported by stringent evidence in humans, and the involvement of several mechanisms rather than just one is also plausible.


Often, people with type 2 diabetes start using insulin with one long-acting shot at night, such as insulin glargine (Lantus) or insulin detemir (Levemir). Discuss the pros and cons of different drugs with your doctor. Together you can decide which medication is best for you after considering many factors, including costs and other aspects of your health.
The typical symptoms of diabetes mellitus are the three “polys:” polyuria, polydipsia, and polyphagia. Because of insulin deficiency, the assimilation and storage of glucose in muscle adipose tissues, and the liver is greatly diminished. This produces an accumulation of glucose in the blood and creates an increase in its osmolarity. In response to this increased osmotic pressure there is depletion of intracellular water and osmotic diuresis. The water loss creates intense thirst and increased urination. The increased appetite (polyphagia) is not as clearly understood. It may be the result of the body's effort to increase its supply of energy foods even though eating more carbohydrates in the absence of sufficient insulin does not meet the energy needs of the cells.
Oral medications are available to lower blood glucose in Type II diabetics. In 1990, 23.4 outpatient prescriptions for oral antidiabetic agents were dispensed. By 2001, the number had increased to 91.8 million prescriptions. Oral antidiabetic agents accounted for more than $5 billion dollars in worldwide retail sales per year in the early twenty-first century and were the fastest-growing segment of diabetes drugs. The drugs first prescribed for Type II diabetes are in a class of compounds called sulfonylureas and include tolbutamide, tolazamide, acetohexamide, and chlorpropamide. Newer drugs in the same class are now available and include glyburide, glimeperide, and glipizide. How these drugs work is not well understood, however, they seem to stimulate cells of the pancreas to produce more insulin. New medications that are available to treat diabetes include metformin, acarbose, and troglitizone. The choice of medication depends in part on the individual patient profile. All drugs have side effects that may make them inappropriate for particular patients. Some for example, may stimulate weight gain or cause stomach irritation, so they may not be the best treatment for someone who is already overweight or who has stomach ulcers. Others, like metformin, have been shown to have positive effects such as reduced cardiovascular mortality, but but increased risk in other situations. While these medications are an important aspect of treatment for Type II diabetes, they are not a substitute for a well planned diet and moderate exercise. Oral medications have not been shown effective for Type I diabetes, in which the patient produces little or no insulin.
The prognosis in people with diabetes varies. It depends on how well an individual modifies his or her risk of complications. If blood sugar is not well controlled, it can increase a person's risk of heart attack, stroke, and kidney disease, which can result in premature death. Disability due to blindness, amputation, heart disease, stroke, and nerve damage may occur. Some people with diabetes become dependent on dialysis treatments because of kidney failure.
You may still feel hungry even after you’ve had something to eat. This is because your tissues aren’t getting enough energy from the food you’ve eaten. If your body is insulin resistant or if your body doesn’t produce enough insulin, the sugar from the food may be unable to enter your tissues to provide energy. This can cause your muscles and other tissues to raise the “hunger flag” in an attempt to get you to eat more food.
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