Type 2 diabetes is due to insufficient insulin production from beta cells in the setting of insulin resistance.[13] Insulin resistance, which is the inability of cells to respond adequately to normal levels of insulin, occurs primarily within the muscles, liver, and fat tissue.[44] In the liver, insulin normally suppresses glucose release. However, in the setting of insulin resistance, the liver inappropriately releases glucose into the blood.[10] The proportion of insulin resistance versus beta cell dysfunction differs among individuals, with some having primarily insulin resistance and only a minor defect in insulin secretion and others with slight insulin resistance and primarily a lack of insulin secretion.[13]
What his theory boils down to is that type 2 diabetes is caused not by extra fat alone, but by fat stored in the wrong places. "Virtually all the individuals [with insulin resistance] have fat accumulation in liver and muscle," Shulman says, where it may disrupt normal biological processes, leading to insulin resistance. "If you can understand this, you can ideally come up with new ways to prevent insulin resistance and type 2 diabetes."
Type 2 DM is characterized by insulin resistance, which may be combined with relatively reduced insulin secretion.[11] The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor. However, the specific defects are not known. Diabetes mellitus cases due to a known defect are classified separately. Type 2 DM is the most common type of diabetes mellitus.[2]
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.
In type 1 diabetes, other symptoms to watch for include unexplained weight loss, lethargy, drowsiness, and hunger. Symptoms sometimes occur after a viral illness. In some cases, a person may reach the point of diabetic ketoacidosis (DKA) before a type 1 diagnosis is made. DKA occurs when blood glucose is dangerously high and the body can't get nutrients into the cells because of the absence of insulin. The body then breaks down muscle and fat for energy, causing an accumulation of ketones in the blood and urine. Symptoms of DKA include a fruity odor on the breath; heavy, taxed breathing; and vomiting. If left untreated, DKA can result in stupor, unconsciousness, and even death.
Individuals with diabetes have two times the likelihood of getting a urinary tract infection compared to individuals without the disease. If you find yourself getting up every couple of hours in the middle of the night, and you seem to be expelling a lot more urine than you used to, talk to your doctor and find out whether or not you have diabetes.

Hyperglycemia or high blood sugar is a serious health problem for diabetics. There are two types of hyperglycemia, 1) fasting, and 2)postprandial or after meal hyperglycemia. Hyperglycemia can also lead to ketoacidosis or hyperglycemic hyperosmolar nonketotic syndrome (HHNS). There are a variety of causes of hyperglycemia in people with diabetes. Symptoms of high blood sugar may include increased thirst, headaches, blurred vision, and frequent urination.Treatment can be achieved through lifestyle changes or medications changes. Carefully monitoring blood glucose levels is key to prevention.

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The causes of diabetes mellitus are unclear, however, there seem to be both hereditary (genetic factors passed on in families) and environmental factors involved. Research has shown that some people who develop diabetes have common genetic markers. In Type I diabetes, the immune system, the body's defense system against infection, is believed to be triggered by a virus or another microorganism that destroys cells in the pancreas that produce insulin. In Type II diabetes, age, obesity, and family history of diabetes play a role.
To explain what hemoglobin A1c is, think in simple terms. Sugar sticks, and when it's around for a long time, it's harder to get it off. In the body, sugar sticks too, particularly to proteins. The red blood cells that circulate in the body live for about three months before they die off. When sugar sticks to these hemoglobin proteins in these cells, it is known as glycosylated hemoglobin or hemoglobin A1c (HBA1c). Measurement of HBA1c gives us an idea of how much sugar is present in the bloodstream for the preceding three months. In most labs, the normal range is 4%-5.9 %. In poorly controlled diabetes, its 8.0% or above, and in well controlled patients it's less than 7.0% (optimal is <6.5%). The benefits of measuring A1c is that is gives a more reasonable and stable view of what's happening over the course of time (three months), and the value does not vary as much as finger stick blood sugar measurements. There is a direct correlation between A1c levels and average blood sugar levels as follows.

n a metabolic disorder caused primarily by a defect in the production of insulin by the islet cells of the pancreas, resulting in an inability to use carbohydrates. Characterized by hyperglycemia, glycosuria, polyuria, hyperlipemia (caused by imperfect catabolism of fats), acidosis, ketonuria, and a lowered resistance to infection. Periodontal manifestations if blood sugar is not being controlled may include recurrent and multiple periodontal abscesses, osteoporotic changes in alveolar bone, fungating masses of granulation tissue protruding from periodontal pockets, a lowered resistance to infection, and delay in healing after periodontal therapy. See also blood glucose level(s).
The pain of diabetic nerve damage may respond to traditional treatments with certain medications such as gabapentin (Neurontin), phenytoin (Dilantin), and carbamazepine (Tegretol) that are traditionally used in the treatment of seizure disorders. Amitriptyline (Elavil, Endep) and desipramine (Norpraminine) are medications that are traditionally used for depression. While many of these medications are not indicated specifically for the treatment of diabetes related nerve pain, they are used by physicians commonly.
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
In an otherwise healthy individual, blood glucose levels usually do not rise above 180 mg/dL (9 mmol/L). In a child with diabetes, blood sugar levels rise if insulin is insufficient for a given glucose load. The renal threshold for glucose reabsorption is exceeded when blood glucose levels exceed 180 mg/dL (10 mmol/L), causing glycosuria with the typical symptoms of polyuria and polydipsia. (See Pathophysiology, Clinical, and Treatment.)
Insulin is a hormone that is produced by specialized cells (beta cells) of the pancreas. (The pancreas is a deep-seated organ in the abdomen located behind the stomach.) In addition to helping glucose enter the cells, insulin is also important in tightly regulating the level of glucose in the blood. After a meal, the blood glucose level rises. In response to the increased glucose level, the pancreas normally releases more insulin into the bloodstream to help glucose enter the cells and lower blood glucose levels after a meal. When the blood glucose levels are lowered, the insulin release from the pancreas is turned down. It is important to note that even in the fasting state there is a low steady release of insulin than fluctuates a bit and helps to maintain a steady blood sugar level during fasting. In normal individuals, such a regulatory system helps to keep blood glucose levels in a tightly controlled range. As outlined above, in patients with diabetes, the insulin is either absent, relatively insufficient for the body's needs, or not used properly by the body. All of these factors cause elevated levels of blood glucose (hyperglycemia).
It is a considerable challenge to obtain the goals of the intensively treated patients in the DCCT with the vast majority of people with diabetes given the more limited health care resources typically available in routine practice. If diabetes control can be improved without significant damage to quality of life, the economic, health, and quality of life savings associated with a reduction in complications in later life will be vast. Although some people who have had poorly controlled diabetes over many years do not develop complications, complications commonly arise after 15–20 years of diabetes and individuals in their 40s or even 30s may develop several complications in rapid succession. However, up until the early 1980s, patients had no way of monitoring their own blood glucose levels at home. Urine glucose monitoring only told them when their blood glucose had exceeded the renal threshold of approximately 10 mmol/L (i.e., was far too high), without being able to discriminate between the too high levels of 7–10 mmol/L or the hypoglycemic levels below 4 mmol/L. Clinics relied on random blood glucose testing and there were no measures of average blood glucose over a longer period. Since the 1980s there have been measures of glycosylated hemoglobin (GHb, HbA1, or HbA1c) which indicate average blood glucose over a six to eight week period and measures of glycosylated protein, fructosamine, which indicates average blood glucose over a two-week period. Blood-glucose meters for patients were first introduced in the early 1980s and the accuracy and convenience of the meters and the reagent strips they use has improved dramatically since early models. By the late 1990s blood-glucose monitoring is part of the daily routine for most people using insulin in developed countries. Blood-glucose monitoring is less often prescribed for tablet- and diet-alone-treated patients, financial reasons probably being allowed to outweigh the educational value of accurate feedback in improving control long term. The reduced risk of hypoglycemia and diabetic ketoacidosis in NIDDM patients not using insulin means that acute crises rarely arise in these patients though their risk of long-term complications is at least as great as in IDDM and might be expected to be reduced if feedback from blood-glucose monitoring were provided.
According to the Mayo Clinic, your risk of developing type 2 diabetes increases as you age. Your risk goes up after age 45 in particular. However, the incidence of type 2 diabetes is increasing dramatically among children, adolescents, and younger adults. Likely factors include reduced exercise, decreased muscle mass, and weight gain as you age. Type 1 diabetes is usually diagnosed by the age of 30.

It is especially important that persons with diabetes who are taking insulin not skip meals; they must also be sure to eat the prescribed amounts at the prescribed times during the day. Since the insulin-dependent diabetic needs to match food consumption to the available insulin, it is advantageous to increase the number of daily feedings by adding snacks between meals and at bedtime.
The patient, physician, nurse, and dietician must carefully evaluate the patient's life style, nutritional needs, and ability to comply with the proposed dietary prescription. There are a variety of meal planning systems that can be used by the patient with diabetes; each has benefits and drawbacks that need to be evaluated in order to maximize compliance. Two of the most frequently used ones are the exchange system (see accompanying table) and the carbohydrate counting system.
How is it treated? There is no uniform therapy for type 2 diabetes treatment, which depends on the individual person and his or her stage of type 2 diabetes. To learn more about individualization of therapy, please read our patient guide. That said, the ADA and EASD have created treatment recommendation guidelines for type 2 diabetes progression. In all cases, healthy eating, exercise, and weight management are key to effective type 2 diabetes management. As type 2 diabetes progresses, patients may need to add one or more drugs to their treatment regimen.
Diabetes mellitus (diabetes) is a common chronic disease of abnormal carbohydrate, fat, and protein metabolism that affects an estimated 20 million people in the United States, of whom about one third are undiagnosed. There are two major forms recognized, type-1 and type-2. Both are characterized by inappropriately high blood sugar levels (hyperglycemia). In type-1 diabetes the patient can not produce the hormone insulin, while in type-2 diabetes the patient produces insulin, but it is not used properly. An estimated 90% of diabetic patients suffer from type-2 disease. The causes of diabetes are multiple and both genetic and environmental factors contribute to its development. The genetic predisposition for type-2 diabetes is very strong and numerous environmental factors such as diet, lack of exercise, and being overweight are known to also increase one’s risk for diabetes. Diabetes is a dangerous disease which affects the entire body and diabetic patients are at increased risk for heart disease, hypertension, stroke, kidney failure, blindness, neuropathy, and infection when compared to nondiabetic patients. Diabetic patients also have impaired healing when compared to healthy individuals. This is in part due to the dysfunction of certain white blood cells that fight infection.
Keep your immunizations up to date. High blood sugar can weaken your immune system. Get a flu shot every year, and your doctor will likely recommend the pneumonia vaccine, as well. The Centers for Disease Control and Prevention (CDC) also recommends the hepatitis B vaccination if you haven't previously received this vaccine and you're an adult age 19 to 59 with type 1 or type 2 diabetes. The CDC advises vaccination as soon as possible after diagnosis with type 1 or type 2 diabetes. If you are age 60 or older, have diabetes and haven't previously received the vaccine, talk to your doctor about whether it's right for you.
The diabetic patient should learn to recognize symptoms of low blood sugar (such as confusion, sweats, and palpitations) and high blood sugar (such as, polyuria and polydipsia). When either condition results in hospitalization, vital signs, weight, fluid intake, urine output, and caloric intake are accurately documented. Serum glucose and urine ketone levels are evaluated. Chronic management of DM is also based on periodic measurement of glycosylated hemoglobin levels (HbA1c). Elevated levels of HbA1c suggest poor long-term glucose control. The effects of diabetes on other body systems (such as cerebrovascular, coronary artery, and peripheral vascular) should be regularly assessed. Patients should be evaluated regularly for retinal disease and visual impairment and peripheral and autonomic nervous system abnormalities, e.g., loss of sensation in the feet. The patient is observed for signs and symptoms of diabetic neuropathy, e.g., numbness or pain in the hands and feet, decreased vibratory sense, footdrop, and neurogenic bladder. The urine is checked for microalbumin or overt protein losses, an early indication of nephropathy. The combination of peripheral neuropathy and peripheral arterial disease results in changes in the skin and microvasculature that lead to ulcer formation on the feet and lower legs with poor healing. Approx. 45,000 lower-extremity diabetic amputations are performed in the U.S. each year. Many amputees have a second amputation within five years. Most of these amputations are preventable with regular foot care and examinations. Diabetic patients and their providers should look for changes in sensation to touch and vibration, the integrity of pulses, capillary refill, and the skin. All injuries, cuts, and blisters should be treated promptly. The patient should avoid constricting hose, slippers, shoes, and bed linens or walking barefoot. The patient with ulcerated or insensitive feet is referred to a podiatrist for continuing foot care and is warned that decreased sensation can mask injuries.
Diagnosis. The most common diagnostic tests for diabetes are chemical analyses of the blood such as the fasting plasma glucose. Capillary blood glucose monitoring can be used for screening large segments of the population. Portable equipment is available and only one drop of blood from the fingertip or earlobe is necessary. Capillary blood glucose levels have largely replaced analysis of the urine for glucose. Testing for urinary glucose can be problematic as the patient may have a high renal threshold, which would lead to a negative reading for urinary glucose when in fact the blood glucose level was high.

Type 2 DM is primarily due to lifestyle factors and genetics.[45] A number of lifestyle factors are known to be important to the development of type 2 DM, including obesity (defined by a body mass index of greater than 30), lack of physical activity, poor diet, stress, and urbanization.[16] Excess body fat is associated with 30% of cases in those of Chinese and Japanese descent, 60–80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders.[11] Even those who are not obese often have a high waist–hip ratio.[11]
Another less common form is gestational diabetes, a temporary condition that occurs during pregnancy. Depending on risk factors, between 3% to 13% of Canadian women will develop gestational diabetes which can be harmful for the baby if not controlled. The problem usually clears up after delivery, but women who have had gestational diabetes have a higher risk of developing type 2 diabetes later in life.
While discovering you have diabetes can be a terrifying prospect, the sooner you’re treated, the more manageable your condition will be. In fact, a review of research published in the American Diabetes Association journal Diabetes Care reveals that early treatment with insulin can help patients with type 2 diabetes manage their blood sugar better and gain less weight than those who start treatment later.
1. Monitoring of blood glucose status. In the past, urine testing was an integral part of the management of diabetes, but it has largely been replaced in recent years by self monitoring of blood glucose. Reasons for this are that blood testing is more accurate, glucose in the urine shows up only after the blood sugar level is high, and individual renal thresholds vary greatly and can change when certain medications are taken. As a person grows older and the kidney is less able to eliminate sugar in the urine, the renal threshold rises and less sugar is spilled into the urine. The position statement of the American Diabetes Association on Tests of Glycemia in Diabetes notes that urine testing still plays a role in monitoring in type 1 and gestational diabetes, and in pregnancy with pre-existing diabetes, as a way to test for ketones. All people with diabetes should test for ketones during times of acute illness or stress and when blood glucose levels are consistently elevated.
Longer-term, the goals of treatment are to prolong life, reduce symptoms, and prevent diabetes-related complications such as blindness, kidney failure, and amputation of limbs. These goals are accomplished through education, insulin use, meal planning and weight control, exercise, foot care, and careful self-testing of blood glucose levels. Self-testing of blood glucose is accomplished through regular use of a blood glucose monitor (pictured, right). This machine can quickly and easily measure the level of blood glucose based by analysing the level from a small drop of blood that is usually obtained from the tip of a finger. You will also require regular tests for glycated haemoglobin (HbA1c). This measures your overall control over several months.

^ 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.
You are more likely to develop type 2 diabetes if you are not physically active and are overweight or obese. Extra weight sometimes causes insulin resistance and is common in people with type 2 diabetes. The location of body fat also makes a difference. Extra belly fat is linked to insulin resistance, type 2 diabetes, and heart and blood vessel disease. To see if your weight puts you at risk for type 2 diabetes, check out these Body Mass Index (BMI) charts.

When you have Type 2 diabetes, you may start out with something called insulin resistance. This means your cells do not respond well to the insulin you are making. "Insulin levels may be quite high, especially in the early stages of the disease. Eventually, your pancreas may not be able to keep up, and insulin secretion goes down," Rettinger explains. Insulin resistance becomes more common as you put on more weight, especially weight around your belly.
Diabetes mellitus results mainly from a deficiency or diminished effectiveness of insulin that is normally produced by the beta cells of the pancreas. It is characterised by high blood sugar, altered sugar and glucose metabolism and this affects blood vessels and causes several organ damage. Causes of diabetes can be classified according to the types of diabetes.
Random blood sugar test. A blood sample will be taken at a random time. Blood sugar values are expressed in milligrams per deciliter (mg/dL) or millimoles per liter (mmol/L). Regardless of when you last ate, a random blood sugar level of 200 mg/dL (11.1 mmol/L) or higher suggests diabetes, especially when coupled with any of the signs and symptoms of diabetes, such as frequent urination and extreme thirst.
Insulin — the hormone that allows your body to regulate sugar in the blood — is made in your pancreas. Essentially, insulin resistance is a state in which the body’s cells do not use insulin efficiently. As a result, it takes more insulin than normal to transport blood sugar (glucose) into cells, to be used immediately for fuel or stored for later use. A drop in efficiency in getting glucose to cells creates a problem for cell function; glucose is normally the body’s quickest and most readily available source of energy.
^ Jump up to: a b Funnell, Martha M.; Anderson, Robert M. (2008). "Influencing self-management: from compliance to collaboration". In Feinglos, Mark N.; Bethel, M. Angelyn. Type 2 diabetes mellitus: an evidence-based approach to practical management. Contemporary endocrinology. Totowa, NJ: Humana Press. p. 462. ISBN 978-1-58829-794-5. OCLC 261324723.

In people with type 1 diabetes, the symptoms often begin abruptly and dramatically. A serious condition called diabetic ketoacidosis, a complication in which the body produces excess acid, may quickly develop. In addition to the usual diabetes symptoms of excessive thirst and urination, the initial symptoms of diabetic ketoacidosis also include nausea, vomiting, fatigue, and—particularly in children—abdominal pain. Breathing tends to become deep and rapid as the body attempts to correct the blood’s acidity (see Acidosis), and the breath smells fruity and like nail polish remover. Without treatment, diabetic ketoacidosis can progress to coma and death, sometimes very quickly.

The most common test used to diagnose diabetes is the fasting blood glucose. This test measures the glucose levels at a specific moment in time (normal is 80-110 mg/dl). In managing diabetes, the goal is to normalize blood glucose levels. It is generally accepted that by maintaining normalized blood glucose levels, one may delay or even prevent some of the complications associated with diabetes. Measures to manage diabetes include behavioral modification (proper diet, exercise) and drug therapies (oral hypoglycemics, insulin replacement). The choice of therapy prescribed takes into consideration the type and severity of the disease present and patient compliance. The physician may request the patient keep a log of their daily blood glucose measurements, in an effort to better assess therapeutic success. Another commonly obtained test is the hemoglobin A1c (HbA1c), which is a surrogate marker used to assess blood glucose levels over an extended period (2-3 months). This test provides the physician with a good picture of the patient’s glucose levels over time.
A study by Chan et al indicated that in pediatric patients with type 1 diabetes, the presence of hypoglycemia is a sign of decreased insulin sensitivity, while hyperglycemia in these patients, especially overnight, signals improved sensitivity to insulin. In contrast, the investigators found evidence that in pediatric patients with type 2 diabetes, markers of metabolic syndrome and hyperglycemia are associated with reduced insulin sensitivity. Patients in the study were between ages 12 and 19 years. [23]
The good news is that prevention plays an important role in warding off these complications. By maintaining tight control of your blood glucose—and getting it as close to normal as possible—you’ll help your body function in the way that it would if you did not have diabetes. Tight control helps you decrease the chances that your body will experience complications from elevated glucose levels.
Previously, CGMs required frequent calibration with fingerstick glucose testing. Also their results were not accurate enough so that people always had to do a fingerstick to verify a reading on their CGM before calculating a dose of insulin (for example before meals or to correct a high blood sugar). However, recent technological advances have improved CGMs. One professional CGM can be worn for up to 14 days without calibration. Another personal CGM can be used to guide insulin dosing without confirmation by fingerstick glucose. Finally, there are now systems in which the CGM device communicates with insulin pumps to either stop delivery of insulin when blood glucose is dropping (threshold suspend), or to give daily insulin (hybrid closed loop system).

The word mellitus (/məˈlaɪtəs/ or /ˈmɛlɪtəs/) comes from the classical Latin word mellītus, meaning "mellite"[114] (i.e. sweetened with honey;[114] honey-sweet[115]). The Latin word comes from mell-, which comes from mel, meaning "honey";[114][115] sweetness;[115] pleasant thing,[115] and the suffix -ītus,[114] whose meaning is the same as that of the English suffix "-ite".[116] It was Thomas Willis who in 1675 added "mellitus" to the word "diabetes" as a designation for the disease, when he noticed the urine of a diabetic had a sweet taste (glycosuria). This sweet taste had been noticed in urine by the ancient Greeks, Chinese, Egyptians, Indians, and Persians.
Type 1 and type 2 diabetes were identified as separate conditions for the first time by the Indian physicians Sushruta and Charaka in 400–500 CE with type 1 associated with youth and type 2 with being overweight.[108] The term "mellitus" or "from honey" was added by the Briton John Rolle in the late 1700s to separate the condition from diabetes insipidus, which is also associated with frequent urination.[108] Effective treatment was not developed until the early part of the 20th century, when Canadians Frederick Banting and Charles Herbert Best isolated and purified insulin in 1921 and 1922.[108] This was followed by the development of the long-acting insulin NPH in the 1940s.[108]
In addition to the problems with an increase in insulin resistance, the release of insulin by the pancreas may also be defective and suboptimal. In fact, there is a known steady decline in beta cell production of insulin in type 2 diabetes that contributes to worsening glucose control. (This is a major factor for many patients with type 2 diabetes who ultimately require insulin therapy.) Finally, the liver in these patients continues to produce glucose through a process called gluconeogenesis despite elevated glucose levels. The control of gluconeogenesis becomes compromised.

A chronic metabolic disorder in which the use of carbohydrate is impaired and that of lipid and protein is enhanced. It is caused by an absolute or relative deficiency of insulin and is characterized, in more severe cases, by chronic hyperglycemia, glycosuria, water and electrolyte loss, ketoacidosis, and coma. Long-term complications include neuropathy, retinopathy, nephropathy, generalized degenerative changes in large and small blood vessels, and increased susceptibility to infection.
Nerve damage from diabetes is called diabetic neuropathy and is also caused by disease of small blood vessels. In essence, the blood flow to the nerves is limited, leaving the nerves without blood flow, and they get damaged or die as a result (a term known as ischemia). Symptoms of diabetic nerve damage include numbness, burning, and aching of the feet and lower extremities. When the nerve disease causes a complete loss of sensation in the feet, patients may not be aware of injuries to the feet, and fail to properly protect them. Shoes or other protection should be worn as much as possible. Seemingly minor skin injuries should be attended to promptly to avoid serious infections. Because of poor blood circulation, diabetic foot injuries may not heal. Sometimes, minor foot injuries can lead to serious infection, ulcers, and even gangrene, necessitating surgical amputation of toes, feet, and other infected parts.
Type 1 and type 2 diabetes were identified as separate conditions for the first time by the Indian physicians Sushruta and Charaka in 400–500 AD with type 1 associated with youth and type 2 with being overweight.[110] The term "mellitus" or "from honey" was added by the Briton John Rolle in the late 1700s to separate the condition from diabetes insipidus which is also associated with frequent urination.[110] Effective treatment was not developed until the early part of the 20th century when the Canadians Frederick Banting and Charles Best discovered insulin in 1921 and 1922.[110] This was followed by the development of the long acting NPH insulin in the 1940s.[110]
With type 1, a disease that often seems to strike suddenly and unexpectedly, the effects of environment and lifestyle are far less clear. But several theories attempt to explain why cases of type 1 have increased so dramatically in recent decades, by around 5 percent per year since 1980. The three main suspects now are too little sun, too good hygiene, and too much cow's milk.
Type 2 DM begins with insulin resistance, a condition in which cells fail to respond to insulin properly.[2] As the disease progresses, a lack of insulin may also develop.[12] This form was previously referred to as "non insulin-dependent diabetes mellitus" (NIDDM) or "adult-onset diabetes".[2] The most common cause is excessive body weight and insufficient exercise.[2]
The blood glucose levels may jump after people eat foods they did not realize were high in carbohydrates. Emotional stress, an infection, and many drugs tend to increase blood glucose levels. Blood glucose levels increase in many people in the early morning hours because of the normal release of hormones (growth hormone and cortisol), a reaction called the dawn phenomenon. Blood glucose may shoot too high if the body releases certain hormones in response to low blood glucose levels (Somogyi effect). Exercise may cause the levels of glucose in the blood to fall low.
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.
The development of type 2 diabetes is caused by a combination of lifestyle and genetic factors.[24][26] While some of these factors are under personal control, such as diet and obesity, other factors are not, such as increasing age, female gender, and genetics.[10] A lack of sleep has been linked to type 2 diabetes.[27] This is believed to act through its effect on metabolism.[27] The nutritional status of a mother during fetal development may also play a role, with one proposed mechanism being that of DNA methylation.[28] The intestinal bacteria Prevotella copri and Bacteroides vulgatus have been connected with type 2 diabetes.[29]
Diabetes mellitus is not a single disorder but a heterogeneous group of disorders. All forms are characterized by hyperglycemia and disturbances of carbohydrate, fat, and protein metabolism which are associated with absolute or relative deficiencies of insulin action and/or insulin secretion. The World Health Organization (WHO) developed a now widely accepted classification of the disorder, largely based on clinical characteristics (see Table 1, WHO, 1985).
The woman’s weight may also play a role. Changing hormone levels and weight gain are part of a healthy pregnancy, but both changes make it more difficult for the body to keep up with its need for insulin. This may lead to gestational diabetes. As pregnancy progresses, the placenta also produces insulin-blocking hormones, which might result in a woman’s blood-glucose levels becoming elevated if there isn’t enough insulin to counter this effect.
While there are competing explanations of the link between obesity and type 2 diabetes, Gerald Shulman, MD, PhD, a professor of internal medicine and physiology at Yale University, believes the key is figuring out insulin resistance. He has studied the causes of insulin resistance for 25 years and thinks he may have the answer to the weight-diabetes link.
Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells. The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (MRDM or MMDM, ICD-10 code E12), was deprecated by the World Health Organization (WHO) when the current taxonomy was introduced in 1999.[53]
A type 2 diabetes diet or a type 2 diabetic diet is important for blood sugar (glucose) control in people with diabetes to prevent complications of diabetes. There are a variety of type 2 diabetes diet eating plans such as the Mediterranean diet, Paleo diet, ADA Diabetes Diet, and vegetarian diets.Learn about low and high glycemic index foods, what foods to eat, and what foods to avoid if you have type 2 diabetes.
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