Findings from the Diabetes Control and Complications Trial (DCCT) and the United Kingdom Prospective Diabetes Study (UKPDS) have clearly shown that aggressive and intensive control of elevated levels of blood sugar in patients with type 1 and type 2 diabetes decreases the complications of nephropathy, neuropathy, retinopathy, and may reduce the occurrence and severity of large blood vessel diseases. Aggressive control with intensive therapy means achieving fasting glucose levels between 70-120 mg/dl; glucose levels of less than 160 mg/dl after meals; and a near normal hemoglobin A1c levels (see below).
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.
Most pediatric patients with diabetes have type 1 diabetes mellitus (T1DM) and a lifetime dependence on exogenous insulin. Diabetes mellitus (DM) is a chronic metabolic disorder caused by an absolute or relative deficiency of insulin, an anabolic hormone. Insulin is produced by the beta cells of the islets of Langerhans located in the pancreas, and the absence, destruction, or other loss of these cells results in type 1 diabetes (insulin-dependent diabetes mellitus [IDDM]). A possible mechanism for the development of type 1 diabetes is shown in the image below. (See Etiology.)
Often people don't experience symptoms of diabetes until their blood sugars are very high. Symptoms of diabetes include: increased thirst, increased urination, increased hunger, extreme fatigues, numbness and tingling in the extremities (hands and feet), cuts and wounds that are slow to heal, and blurred vision. Some people also experience other less common symptoms including weight loss, dry itchy skin, increased yeast infections, erectile dysfunction, and acanthosis nigricans (thick, "velvety" patches found in the folds or creases of skin, such as the neck, that is indicative of insulin resistance).
It will surely be tough eating salads and vegetables when everyone else at your dinner table is eating pizza. Decide that this diagnosis can benefit the health of the entire family. Educate your family about the benefits of eating a healthy diet. Take your children grocery shopping with you. Practice the plate method: Aim to make half your plate non-starchy vegetables; a quarter lean protein; and a quarter whole grains or starchy vegetables, like sweet potatoes. Make exercise part of your daily routine and include your family. Go for walks after dinner. Head to the pool on the weekends, or enroll in an exercise class. If you don't have children, aim to find others with diabetes or friends that can act as your workout partners.

The amount of glucose in the bloodstream is tightly regulated by insulin and other hormones. Insulin is always being released in small amounts by the pancreas. When the amount of glucose in the blood rises to a certain level, the pancreas will release more insulin to push more glucose into the cells. This causes the glucose levels in the blood (blood glucose levels) to drop.


Awareness about the signs and symptoms and periodic screening especially in the presence of risk factors and warning signs of diabetes, would go a long way in preventing new cases of diabetes by providing an opportunity to intervene at the stage of prediabetes. It is evident that diabetes can be prevented among prediabetic individuals by improvements in physical activity and diet habits. Such strategies will also prevent development of diabetic complications to a great extent. Patient empowerment is vital in diabetes management. This can be done through patient education and sharing information on management and preventive aspects of diabetes.
By simultaneously considering insulin secretion and insulin action in any given individual, it becomes possible to account for the natural history of diabetes in that person (e.g., remission in a patient with T1 diabetes or ketoacidosis in a person with T2DM). Thus, diabetes mellitus may be the result of absolute insulin deficiency, or of absolute insulin resistance, or a combination of milder defects in both insulin secretion and insulin action.1 Collectively, the syndromes of diabetes mellitus are the most common endocrine/metabolic disorders of childhood and adolescence. The application of molecular biologic tools continues to provide remarkable insights into the etiology, pathophysiology, and genetics of the various forms of diabetes mellitus that result from deficient secretion of insulin or its action at the cellular level.
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
Rates of diabetes in 1985 were estimated at 30 million, increasing to 135 million in 1995 and 217 million in 2005.[18] This increase is believed to be primarily due to the global population aging, a decrease in exercise, and increasing rates of obesity.[18] The five countries with the greatest number of people with diabetes as of 2000 are India having 31.7 million, China 20.8 million, the United States 17.7 million, Indonesia 8.4 million, and Japan 6.8 million.[109] It is recognized as a global epidemic by the World Health Organization.[1]
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.
Type 2 (formerly called 'adult-onset' or 'non insulin-dependent') diabetes results when the body doesn’t produce enough insulin and/or is unable to use insulin properly (this is also referred to as ‘insulin resistance’). This form of diabetes usually occurs in people who are over 40 years of age, overweight, and have a family history of diabetes, although today it is increasingly found in younger people.
Type 1 diabetes mellitus has wide geographic variation in incidence and prevalence. [30] Annual incidence varies from 0.61 cases per 100,000 population in China to 41.4 cases per 100,000 population in Finland. Substantial variations are observed between nearby countries with differing lifestyles, such as Estonia and Finland, and between genetically similar populations, such as those in Iceland and Norway.
The 1989 "St. Vincent Declaration"[117][118] was the result of international efforts to improve the care accorded to those with diabetes. Doing so is important not only in terms of quality of life and life expectancy but also economically – expenses due to diabetes have been shown to be a major drain on health – and productivity-related resources for healthcare systems and governments.

It’s no surprise that most people could stand to drink more water. In fact, the majority of Americans are drinking less than half of the recommended eight glasses of water each day. However, if you’re finding yourself excessively thirsty, that could be a sign that you’re dealing with dangerously high blood sugar. Patients with diabetes often find themselves extremely thirsty as their bodies try to flush out excess sugar in their blood when their own insulin production just won’t cut it. If you’re parched, instead of turning to a sugary drink, quench that thirst with one of the 50 Best Detox Waters for Fat Burning and Weight Loss!
Because type 2 diabetes is linked to high levels of sugar in the blood, it may seem logical to assume that eating too much sugar is the cause of the disease. But of course, it’s not that simple. “This has been around for years, this idea that eating too much sugar causes diabetes — but the truth is, type 2 diabetes is a multifactorial disease with many different types of causes,” says Lynn Grieger, RDN, CDE, a nutrition coach in Prescott, Arizona, and a medical reviewer for Everyday Health. “Type 2 diabetes is really complex.”
How does type 2 diabetes progress over time? Type 2 diabetes is a progressive disease, meaning that the body’s ability to regulate blood sugar gets worse over time, despite careful management. Over time, the body’s cells become increasingly less responsive to insulin (increased insulin resistance) and beta cells in the pancreas produce less and less insulin (called beta-cell burnout). In fact, when people are diagnosed with type 2 diabetes, they usually have already lost up to 50% or more of their beta cell function. As type 2 diabetes progresses, people typically need to add one or more different types of medications. The good news is that there are many more choices available for treatments, and a number of these medications don’t cause as much hypoglycemia, hunger and/or weight gain (e.g., metformin, pioglitazone, DPP-4 inhibitors, GLP-1 agonists, SGLT-2 inhibitors, and better insulin). Diligent management early on can help preserve remaining beta cell function and sometimes slow progression of the disease, although the need to use more and different types of medications does not mean that you have failed.
Type 2 diabetes is believed to have a strong genetic link, meaning that it tends to run in families. Several genes are being studied that may be related to the cause of type 2 diabetes. If you have any of the following type 2 diabetes risk factors, it’s important to ask your doctor about a diabetes test. With a proper diabetes diet and healthy lifestyle habits, along with diabetes medication, if necessary, you can manage type 2 diabetes just like you manage other areas of your life. Be sure to continue seeking the latest information on type 2 diabetes as you become your own health advocate.

The term "type 1 diabetes" has replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus (IDDM). Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and noninsulin-dependent diabetes mellitus (NIDDM). Beyond these two types, there is no agreed-upon standard nomenclature.[citation needed]
Kidney damage from diabetes is called diabetic nephropathy. The onset of kidney disease and its progression is extremely variable. Initially, diseased small blood vessels in the kidneys cause the leakage of protein in the urine. Later on, the kidneys lose their ability to cleanse and filter blood. The accumulation of toxic waste products in the blood leads to the need for dialysis. Dialysis involves using a machine that serves the function of the kidney by filtering and cleaning the blood. In patients who do not want to undergo chronic dialysis, kidney transplantation can be considered.
For Candace Clark, bariatric surgery meant the difference between struggling with weight issues, including medical problems triggered by obesity, and enjoying renewed health and energy. "I felt like I was slowly dying," says Candace Clark, a 54-year-old Barron, Wisconsin, resident who had dealt with weight issues for years. "I was tired of feeling the way [...]
The progression of nephropathy in patients can be significantly slowed by controlling high blood pressure, and by aggressively treating high blood sugar levels. Angiotensin converting enzyme inhibitors (ACE inhibitors) or angiotensin receptor blockers (ARBs) used in treating high blood pressure may also benefit kidney disease in patients with diabetes.

The ADA recommends using patient age as one consideration in the establishment of glycemic goals, with different targets for preprandial, bedtime/overnight, and hemoglobin A1c (HbA1c) levels in patients aged 0-6, 6-12, and 13-19 years. [4] Benefits of tight glycemic control include not only continued reductions in the rates of microvascular complications but also significant differences in cardiovascular events and overall mortality.
Type 2 diabetes is one of the major degenerative diseases in the Western world today. It happens when your body can’t use insulin properly, or can’t make enough insulin. Insulin is a hormone the assists the body’s cells in utilizing glucose. It also helps the body store extra sugar in fat, liver, and muscle cells. If you don’t have insulin, your body can’t use the sugar in the bloodstream.

Sequelae. The long-term consequences of diabetes mellitus can involve both large and small blood vessels throughout the body. That in large vessels is usually seen in the coronary arteries, cerebral arteries, and arteries of the lower extremities and can eventually lead to myocardial infarction, stroke, or gangrene of the feet and legs. atherosclerosis is far more likely to occur in persons of any age who have diabetes than it is in other people. This predisposition is not clearly understood. Some believe that diabetics inherit the tendency to develop severe atherosclerosis as well as an aberration in glucose metabolism, and that the two are not necessarily related. There is strong evidence to substantiate the claim that optimal control will mitigate the effects of diabetes on the microvasculature, particularly in the young and middle-aged who are at greatest risk for developing complications involving the arterioles. Pathologic changes in the small blood vessels serving the kidney lead to nephrosclerosis, pyelonephritis, and other disorders that eventually result in renal failure. Many of the deaths of persons with type 1 diabetes are caused by renal failure.
People with type 1 diabetes are unable to produce any insulin at all. People with type 2 diabetes still produce insulin, however, the cells in the muscles, liver and fat tissue are inefficient at absorbing the insulin and cannot regulate glucose well. As a result, the body tries to compensate by having the pancreas pump out more insulin. But the pancreas slowly loses the ability to produce enough insulin, and as a result, the cells don’t get the energy they need to function properly.
^ Jump up to: a b c Maruthur, NM; Tseng, E; Hutfless, S; Wilson, LM; Suarez-Cuervo, C; Berger, Z; Chu, Y; Iyoha, E; Segal, JB; Bolen, S (19 April 2016). "Diabetes Medications as Monotherapy or Metformin-Based Combination Therapy for Type 2 Diabetes: A Systematic Review and Meta-analysis". Annals of Internal Medicine. 164 (11): 740–51. doi:10.7326/M15-2650. PMID 27088241.

Say that two people have the same genetic mutation. One of them eats well, watches their cholesterol, and stays physically fit, and the other is overweight (BMI greater than 25) and inactive. The person who is overweight and inactive is much more likely to develop type 2 diabetes because certain lifestyle choices greatly influence how well your body uses insulin.


Hyperglycemia (ie, random blood glucose concentration of more than 200 mg/dL or 11 mmol/L) results when insulin deficiency leads to uninhibited gluconeogenesis and prevents the use and storage of circulating glucose. The kidneys cannot reabsorb the excess glucose load, causing glycosuria, osmotic diuresis, thirst, and dehydration. Increased fat and protein breakdown leads to ketone production and weight loss. Without insulin, a child with type 1 diabetes mellitus wastes away and eventually dies due to DKA. The effects of insulin deficiency are shown in the image below.
Diabetes mellitus (“diabetes”) and hypertension, which commonly coexist, are global public health issues contributing to an enormous burden of cardiovascular disease, chronic kidney disease, and premature mortality and disability. The presence of both conditions has an amplifying effect on risk for microvascular and macrovascular complications.1 The prevalence of diabetes is rising worldwide (Fig. 37.1). Both diabetes and hypertension disproportionately affect people in middle and low-income countries, and an estimated 70% of all cases of diabetes are found in these countries.2,3 In the United States alone, the total costs of care for diabetes and hypertension in the years 2012 and 2011 were 245 and 46 billion dollars, respectively.4,5 Therefore, there is a great potential for meaningful health and economic gains attached to prevention, detection, and intervention for diabetes and hypertension.
Inhalable insulin has been developed.[125] The original products were withdrawn due to side effects.[125] Afrezza, under development by the pharmaceuticals company MannKind Corporation, was approved by the United States Food and Drug Administration (FDA) for general sale in June 2014.[126] An advantage to inhaled insulin is that it may be more convenient and easy to use.[127]
Diabetes mellitus is a chronic disease caused by inherited and/or acquired deficiency in production of insulin by the pancreas, or by the ineffectiveness of the insulin produced. Such a deficiency results in increased concentrations of glucose in the blood, which in turn damage many of the body's systems, in particular the blood vessels and nerves.
There are a number of medications and other health problems that can predispose to diabetes.[39] Some of the medications include: glucocorticoids, thiazides, beta blockers, atypical antipsychotics,[40] and statins.[41] Those who have previously had gestational diabetes are at a higher risk of developing type 2 diabetes.[23] Other health problems that are associated include: acromegaly, Cushing's syndrome, hyperthyroidism, pheochromocytoma, and certain cancers such as glucagonomas.[39] Testosterone deficiency is also associated with type 2 diabetes.[42][43]
The treatment of low blood sugar consists of administering a quickly absorbed glucose source. These include glucose containing drinks, such as orange juice, soft drinks (not sugar-free), or glucose tablets in doses of 15-20 grams at a time (for example, the equivalent of half a glass of juice). Even cake frosting applied inside the cheeks can work in a pinch if patient cooperation is difficult. If the individual becomes unconscious, glucagon can be given by intramuscular injection.
Constant advances are being made in development of new oral medications for persons with diabetes. In 2003, a drug called Metaglip combining glipizide and metformin was approved in a dingle tablet. Along with diet and exercise, the drug was used as initial therapy for Type 2 diabetes. Another drug approved by the U.S. Food and Drug Administration (FDA) combines metformin and rosiglitazone (Avandia), a medication that increases muscle cells' sensitivity to insulin. It is marketed under the name Avandamet. So many new drugs are under development that it is best to stay in touch with a physician for the latest information; physicians can find the best drug, diet and exercise program to fit an individual patient's need.
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.
The body will attempt to dilute the high level of glucose in the blood, a condition called hyperglycemia, by drawing water out of the cells and into the bloodstream in an effort to dilute the sugar and excrete it in the urine. It is not unusual for people with undiagnosed diabetes to be constantly thirsty, drink large quantities of water, and urinate frequently as their bodies try to get rid of the extra glucose. This creates high levels of glucose in the urine.

Dr. Balentine received his undergraduate degree from McDaniel College in Westminster, Maryland. He attended medical school at the Philadelphia College of Osteopathic Medicine graduating in1983. He completed his internship at St. Joseph's Hospital in Philadelphia and his Emergency Medicine residency at Lincoln Medical and Mental Health Center in the Bronx, where he served as chief resident.
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.
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

This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. The NIDDK translates and disseminates research findings through its clearinghouses and education programs to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by the NIDDK is carefully reviewed by NIDDK scientists and other experts.

Type 2 diabetes is one of the major degenerative diseases in the Western world today. It happens when your body can’t use insulin properly, or can’t make enough insulin. Insulin is a hormone the assists the body’s cells in utilizing glucose. It also helps the body store extra sugar in fat, liver, and muscle cells. If you don’t have insulin, your body can’t use the sugar in the bloodstream.

Per the WHO, people with fasting glucose levels from 6.1 to 6.9 mmol/l (110 to 125 mg/dl) are considered to have impaired fasting glucose.[67] people with plasma glucose at or above 7.8 mmol/l (140 mg/dl), but not over 11.1 mmol/l (200 mg/dl), two hours after a 75 gram oral glucose load are considered to have impaired glucose tolerance. Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease.[68] The American Diabetes Association (ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/l (100 to 125 mg/dl).[69]


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.
Because people with type 2 diabetes produce some insulin, ketoacidosis does not usually develop even when type 2 diabetes is untreated for a long time. Rarely, the blood glucose levels become extremely high (even exceeding 1,000 mg/dL). Such high levels often happen as the result of some superimposed stress, such as an infection or drug use. When the blood glucose levels get very high, people may develop severe dehydration, which may lead to mental confusion, drowsiness, and seizures, a condition called hyperosmolar hyperglycemic state. Currently, many people with type 2 diabetes are diagnosed by routine blood glucose testing before they develop such severely high blood glucose levels.
Type 1 diabetes has some connection to your family genes, but that doesn't mean you'll get it if one of your parents had it. "Since not all identical twins get diabetes, we do think that exposure to an additional environmental factor may trigger an immune response that ultimately causes destruction of the insulin-producing cells of the pancreas," says Dr. Sarah R. Rettinger, an endocrinologist with Providence Saint John's Health Center in Santa Monica, California.

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.)


The most common cause of acquired blindness in many developed nations, diabetic retinopathy is rare in the prepubertal child or within 5 years of onset of diabetes. The prevalence and severity of retinopathy increase with age and are greatest in patients whose diabetic control is poor. [14] Prevalence rates seem to be declining, yet an estimated 80% of people with type 1 diabetes mellitus develop retinopathy. [15]
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.
×