observations The onset of type 1 diabetes mellitus is sudden in children. Type 2 diabetes often begins insidiously. Characteristically the course is progressive and includes polyuria, polydipsia, weight loss, polyphagia, hyperglycemia, and glycosuria. The eyes, kidneys, nervous system, skin, and circulatory system may be affected by the long-term complications of either type of diabetes; infections are common; and atherosclerosis often develops. In type 1 diabetes mellitus, when no endogenous insulin is being secreted, ketoacidosis is a constant danger. The diagnosis is confirmed by fasting plasma glucose and history.
Diabetes that's triggered by pregnancy is called gestational diabetes (pregnancy, to some degree, leads to insulin resistance). It is often diagnosed in middle or late pregnancy. Because high blood sugar levels in a mother are circulated through the placenta to the baby, gestational diabetes must be controlled to protect the baby's growth and development.
Several tests are helpful in identifying DM. These include tests of fasting plasma glucose levels, casual (randomly assessed) glucose levels, or glycosylated hemoglobin levels. Diabetes is currently established if patients have classic diabetic symptoms and if on two occasions fasting glucose levels exceed 126 mg/dL (> 7 mmol/L), random glucose levels exceed 200 mg/dL (11.1 mmol/L), or a 2-hr oral glucose tolerance test is 200 mg/dL or more. A hemoglobin A1c test that is more than two standard deviations above normal (6.5% or greater) is also diagnostic of the disease.

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

Beta cells are vulnerable to more than just bad genes, which may explain the associations between type 2 diabetes and environmental factors that aren't related to how much fat a body has or where it is stored. Beta cells carry vitamin D receptors on their surface, and people with vitamin D deficiency are at increased risk for type 2. Plus, several studies have shown that people with higher levels of toxic substances in their blood—such as from the PCBs found in fish fat—are at increased risk of type 2 diabetes, though a cause-and-effect relationship hasn't been proved. (Toxic substances and vitamin D have also been implicated in type 1 diabetes, but the disease mechanism may be unrelated to what's going on in type 2.)
Jump up ^ Seida, Jennifer C.; Mitri, Joanna; Colmers, Isabelle N.; Majumdar, Sumit R.; Davidson, Mayer B.; Edwards, Alun L.; Hanley, David A.; Pittas, Anastassios G.; Tjosvold, Lisa; Johnson, Jeffrey A. (Oct 2014). "Effect of Vitamin D3 Supplementation on Improving Glucose Homeostasis and Preventing Diabetes: A Systematic Review and Meta-Analysis". The Journal of Clinical Endocrinology & Metabolism. 99 (10): 3551–60. doi:10.1210/jc.2014-2136. PMC 4483466. PMID 25062463.
Onset of type 2 diabetes can be delayed or prevented through proper nutrition and regular exercise.[60][61] Intensive lifestyle measures may reduce the risk by over half.[24][62] The benefit of exercise occurs regardless of the person's initial weight or subsequent weight loss.[63] High levels of physical activity reduce the risk of diabetes by about 28%.[64] Evidence for the benefit of dietary changes alone, however, is limited,[65] with some evidence for a diet high in green leafy vegetables[66] and some for limiting the intake of sugary drinks.[32] In those with impaired glucose tolerance, diet and exercise either alone or in combination with metformin or acarbose may decrease the risk of developing diabetes.[24][67] Lifestyle interventions are more effective than metformin.[24] A 2017 review found that, long term, lifestyle changes decreased the risk by 28%, while medication does not reduce risk after withdrawal.[68] While low vitamin D levels are associated with an increased risk of diabetes, correcting the levels by supplementing vitamin D3 does not improve that risk.[69]
Type I diabetes, sometimes called juvenile diabetes, begins most commonly in childhood or adolescence. In this form of diabetes, the body produces little or no insulin. It is characterized by a sudden onset and occurs more frequently in populations descended from Northern European countries (Finland, Scotland, Scandinavia) than in those from Southern European countries, the Middle East, or Asia. In the United States, approximately three people in 1,000 develop Type I diabetes. This form also is called insulin-dependent diabetes because people who develop this type need to have daily injections of insulin.
Assemble a Medical Team: Whether you've had diabetes for a long time or you've just been diagnosed, there are certain doctors that are important to see. It is extremely important to have a good primary care physician. This type of doctor will help coordinate appointments for other physicians if they think that you need it. Some primary physicians treat diabetes themselves, whereas others will recommend that you visit an endocrinologist for diabetes treatment. An endocrinologist is a person who specializes in diseases of the endocrine system, diabetes being one of them.

Insulin inhibits glucogenesis and glycogenolysis, while stimulating glucose uptake. In nondiabetic individuals, insulin production by the pancreatic islet cells is suppressed when blood glucose levels fall below 83 mg/dL (4.6 mmol/L). If insulin is injected into a treated child with diabetes who has not eaten adequate amounts of carbohydrates, blood glucose levels progressively fall.

There is currently no cure for diabetes. The condition, however, can be managed so that patients can live a relatively normal life. Treatment of diabetes focuses on two goals: keeping blood glucose within normal range and preventing the development of long-term complications. Careful monitoring of diet, exercise, and blood glucose levels are as important as the use of insulin or oral medications in preventing complications of diabetes. In 2003, the American Diabetes Association updated its Standards of Care for the management of diabetes. These standards help manage health care providers in the most recent recommendations for diagnosis and treatment of the disease.
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]

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
Type 2 diabetes is different. A person with type 2 diabetes still produces insulin but the body doesn't respond to it normally. Glucose is less able to enter the cells and do its job of supplying energy (a problem called insulin resistance). This raises the blood sugar level, so the pancreas works hard to make even more insulin. Eventually, this strain can make the pancreas unable to produce enough insulin to keep blood sugar levels normal.

The term brittle diabetes has been used to refer to people who have dramatic recurrent swings in blood glucose levels, often for no apparent reason. However, this term is no longer used. People with type 1 diabetes may have more frequent swings in blood glucose levels because insulin production is completely absent. Infection, delayed movement of food through the stomach, and other hormonal disorders may also contribute to blood glucose swings. In all people who have difficulty controlling blood glucose, doctors look for other disorders that might be causing the problem and also give people additional education on how to monitor diabetes and take their drugs.

Type 1 diabetes is considered an autoimmune disease. With an autoimmune disease, your immune system – which helps protect your body from getting sick – is engaged in too little or too much activity. In Type 1 diabetes, beta cells, which are a kind of cell in the pancreas that produces insulin, are destroyed. Our bodies use insulin to take the sugar from carbohydrates we eat and create fuel. With Type 1 diabetes, your body does not produce insulin, and that's why you need to use insulin as part of your treatment.

The good news is that if you have diabetes, you have a great amount of control in managing your disease. Although it can be difficult to manage a disease on a daily basis, the resources and support for people with diabetes is endless. It's important for you to receive as much education as possible so that you can take advantage of all the good information that is out there (and weed out the bad).


The primary complications of diabetes due to damage in small blood vessels include damage to the eyes, kidneys, and nerves.[32] Damage to the eyes, known as diabetic retinopathy, is caused by damage to the blood vessels in the retina of the eye, and can result in gradual vision loss and eventual blindness.[32] Diabetes also increases the risk of having glaucoma, cataracts, and other eye problems. It is recommended that diabetics visit an eye doctor once a year.[33] Damage to the kidneys, known as diabetic nephropathy, can lead to tissue scarring, urine protein loss, and eventually chronic kidney disease, sometimes requiring dialysis or kidney transplantation.[32] Damage to the nerves of the body, known as diabetic neuropathy, is the most common complication of diabetes.[32] The symptoms can include numbness, tingling, pain, and altered pain sensation, which can lead to damage to the skin. Diabetes-related foot problems (such as diabetic foot ulcers) may occur, and can be difficult to treat, occasionally requiring amputation. Additionally, proximal diabetic neuropathy causes painful muscle atrophy and weakness.
Other potentially important mechanisms associated with type 2 diabetes and insulin resistance include: increased breakdown of lipids within fat cells, resistance to and lack of incretin, high glucagon levels in the blood, increased retention of salt and water by the kidneys, and inappropriate regulation of metabolism by the central nervous system.[10] However, not all people with insulin resistance develop diabetes, since an impairment of insulin secretion by pancreatic beta cells is also required.[13]
^ Jump up to: a b Cheng, J; Zhang, W; Zhang, X; Han, F; Li, X; He, X; Li, Q; Chen, J (May 2014). "Effect of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers on all-cause mortality, cardiovascular deaths, and cardiovascular events in patients with diabetes mellitus: a meta-analysis". JAMA Internal Medicine. 174 (5): 773–85. doi:10.1001/jamainternmed.2014.348. PMID 24687000.
A person of Asian origin aged 35 yr or more with two or more of the above risk factors, should undergo a screening test for diabetes. An oral glucose tolerance test (OGTT) is commonly used as the screening test10. Fasting and 2 h post glucose tests can identify impaired fasting glucose (IFG) (fasting glucose >110 - <125 mg/dl), impaired glucose tolerance (IGT) (2 h glucose >140-<200 mg/dl) and presence of diabetes (fasting > 126 and 2 h glucose >200 mg/dl). If a random blood glucose value is > 150 mg/dl, further confirmation by an OGTT is warranted. Recently, glycosylated haemoglobin (HbA1c) has been recommended as the test for diagnosis of diabetes (>6.5%). Presence of pre-diabetes is indicated by HbA1c values between 5.7 - 6.4 per cent11.
This is specific to type 2 diabetes. It occurs when insulin is produced normally in the pancreas, but the body is still unable move glucose into the cells for fuel. At first, the pancreas will create more insulin to overcome the body’s resistance. Eventually the cells “wear out.” At that point the body slows insulin production, leaving too much glucose in the blood. This is known as prediabetes. A person with prediabetes has a blood sugar level higher than normal but not high enough for a diagnosis of diabetes. Unless tested, the person may not be aware, as there are no clear symptoms. Type 2 diabetes occurs as insulin production continues to decrease and resistance increases.

Know Your Numbers: Knowing your ABCs—A1c, blood pressure, and cholesterol—are important in reducing your risk for diabetes and keeping your diabetes in good control. If you are someone with diabetes who has elevated blood pressure or cholesterol, you are increasing your risk of heart attack and stroke. Your physician will give you your A1c, blood pressure, and cholesterol targets. Make sure you pay attention to them and understand what they mean and why they are important.
Diabetes is a metabolic disorder that occurs when your blood sugar (glucose), is too high (hyperglycemia). Glucose is what the body uses for energy, and the pancreas produces a hormone called insulin that helps convert the glucose from the food you eat into energy. When the body does not produce enough insulin - or does not produce any at all - the glucose does not reach your cells to be used for energy. This results in diabetes.

Type 2 diabetes usually has a slower onset and can often go undiagnosed. But many people do have symptoms like extreme thirst and frequent urination. Other signs include sores that won't heal, frequent infections (including vaginal infections in some women), and changes in vision. Some patients actually go to the doctor with symptoms resulting from the complications of diabetes, like tingling in the feet (neuropathy) or vision loss (retinopathy), without knowing they have the disease. This is why screening people at risk for diabetes is so important. The best way to avoid complications is to get blood glucose under control before

Insulin works like a key that opens the doors to cells and lets the glucose in. Without insulin, glucose can't get into the cells (the doors are "locked" and there is no key) and so it stays in the bloodstream. As a result, the level of sugar in the blood remains higher than normal. High blood sugar levels are a problem because they can cause a number of health problems.
While this can produce different types of complications, good blood sugar control efforts can help to prevent them. This relies heavily on lifestyle modifications such as weight loss, dietary changes, exercise and, in some cases, medication. But, depending on your age, weight, blood sugar level, and how long you've had diabetes, you may not need a prescription right away. Treatment must be tailored to you and, though finding the perfect combination may take a little time, it can help you live a healthy, normal life with diabetes.
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
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