The most common complication of treating high blood glucose levels is low blood glucose levels (hypoglycemia). The risk is greatest for older people who are frail, who are sick enough to require frequent hospital admissions, or who are taking several drugs. Of all available drugs to treat diabetes, long-acting sulfonylurea drugs are most likely to cause low blood glucose levels in older people. When they take these drugs, they are also more likely to have serious symptoms, such as fainting and falling, and to have difficulty thinking or using parts of the body due to low blood glucose levels.
In type 2 diabetes (formerly called non– insulin-dependent diabetes or adult-onset diabetes), the pancreas often continues to produce insulin, sometimes even at higher-than-normal levels, especially early in the disease. However, the body develops resistance to the effects of insulin, so there is not enough insulin to meet the body’s needs. As type 2 diabetes progresses, the insulin-producing ability of the pancreas decreases.

Although there are dozens of known type 1 genes, about half of the risk attributable to heredity comes from a handful that coordinate a part of the immune system called HLA, which helps the body recognize nefarious foreign invaders, such as viruses, bacteria, and parasites. Type 1 diabetes is an autoimmune disease, in which the body's own immune system destroys the cells in the pancreas that produce insulin, so perhaps it is no surprise that immunity genes are involved. Other autoimmune diseases share the HLA gene link, which may be why people with type 1 are more likely to develop additional auto­immune disorders.
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.

Type 2 diabetes typically starts with insulin resistance. That is, the cells of the body resist insulin’s efforts to escort glucose into the cells. What causes insulin resistance? It appears to be caused by an accumulation of microscopic fat particles within muscle and liver cells.4 This fat comes mainly from the diet—chicken fat, beef fat, cheese fat, fish fat, and even vegetable fat. To try to overcome insulin resistance, the pancreas produces extra insulin. When the pancreas can no longer keep up, blood sugar rises. The combination of insulin resistance and pancreatic cell failure leads to type 2 diabetes.
Dr. Shiel received a Bachelor of Science degree with honors from the University of Notre Dame. There he was involved in research in radiation biology and received the Huisking Scholarship. After graduating from St. Louis University School of Medicine, he completed his Internal Medicine residency and Rheumatology fellowship at the University of California, Irvine. He is board-certified in Internal Medicine and Rheumatology.
Low glycemic index foods also may be helpful. The glycemic index is a measure of how quickly a food causes a rise in your blood sugar. Foods with a high glycemic index raise your blood sugar quickly. Low glycemic index foods may help you achieve a more stable blood sugar. Foods with a low glycemic index typically are foods that are higher in fiber.

What are the symptoms of diabetes in women? Diabetes can have different effects on men and women. Learn all about the symptoms of diabetes experienced by women with this article, including how the disease may affect pregnancy and the menopause. This MNT Knowledge Center article will also look at gestational diabetes and the risk factors involved. Read now
If eaten as part of a healthy meal plan, or combined with exercise, sweets and desserts can be eaten by people with diabetes. They are no more "off limits" to people with diabetes than they are to people without diabetes. The key to sweets is to have a very small portion and save them for special occasions so you focus your meal on more healthful foods.
Adrenal Disease Chapter Anatomy Chapter Dermatology Chapter Diabetes Mellitus Chapter Examination Chapter Gastroenterology Chapter General Chapter Geriatric Medicine Chapter Growth Disorders Chapter Hematology and Oncology Chapter Hypoglycemic Disorders Chapter Infectious Disease Chapter Metabolic Disorders Chapter Neonatology Chapter Nephrology Chapter Neurology Chapter Obesity Chapter Obstetrics Chapter Ophthalmology Chapter Parathyroid Disease Chapter Pathology and Laboratory Medicine Chapter Pediatrics Chapter Pharmacology Chapter Pituitary Disease Chapter Prevention Chapter Radiology Chapter Sexual Development Chapter Sports Medicine Chapter Surgery Chapter Symptoms Chapter Thyroid Disease Chapter
Diabetes mellitus is a diagnostic term for a group of disorders characterized by abnormal glucose homeostasis resulting in elevated blood sugar. There is variability in its manifestations, wherein some individuals have only asymptomatic glucose intolerance, while others present acutely with diabetic ketoacidosis, and still others develop chronic complications such as nephropathy, neuropathy, retinopathy, or accelerated atherosclerosis. It is among the most common of chronic disorders, affecting up to 5–10% of the adult population of the Western world. Its prevalence varies over the globe, with certain populations, including some American Indian tribes and the inhabitants of Micronesia and Polynesia, having extremely high rates of diabetes (1,2). The prevalence of diabetes is increasing dramatically and it has been estimated that the worldwide prevalence will increase by more than 50% between the years 2000 and 2030 (3).
It is clearly established that diabetes mellitus is not a single disease but a genetically heterogeneous group of disorders that share glucose intolerance in common (4–7). The concept of genetic heterogeneity (i.e. that different genetic and/or environmental etiologic factors can result in similar phenotypes) has significantly altered the genetic analysis of this common disorder. Diabetes and glucose intolerance are not diagnostic terms, but, like anemia, simply describe symptoms and/or laboratory abnormalities that can have a number of distinct etiologies.
Low blood sugar (hypoglycemia), is common in people with type 1 and type 2 DM. Most cases are mild and are not considered medical emergencies. Effects can range from feelings of unease, sweating, trembling, and increased appetite in mild cases to more serious effects such as confusion, changes in behavior such as aggressiveness, seizures, unconsciousness, and (rarely) permanent brain damage or death in severe cases.[24][25] Moderately low blood sugar may easily be mistaken for drunkenness;[26] rapid breathing and sweating, cold, pale skin are characteristic of low blood sugar but not definitive.[27] Mild to moderate cases are self-treated by eating or drinking something high in sugar. Severe cases can lead to unconsciousness and must be treated with intravenous glucose or injections with glucagon.[28]
In animals, diabetes is most commonly encountered in dogs and cats. Middle-aged animals are most commonly affected. Female dogs are twice as likely to be affected as males, while according to some sources, male cats are also more prone than females. In both species, all breeds may be affected, but some small dog breeds are particularly likely to develop diabetes, such as Miniature Poodles.[123]
Diabetes mellitus is a disorder in which the amount of sugar in the blood is elevated. Doctors often use the full name diabetes mellitus, rather than diabetes alone, to distinguish this disorder from diabetes insipidus. Diabetes insipidus is a relatively rare disorder that does not affect blood glucose levels but, just like diabetes mellitus, also causes increased urination.
Dr. Charles "Pat" Davis, MD, PhD, is a board certified Emergency Medicine doctor who currently practices as a consultant and staff member for hospitals. He has a PhD in Microbiology (UT at Austin), and the MD (Univ. Texas Medical Branch, Galveston). He is a Clinical Professor (retired) in the Division of Emergency Medicine, UT Health Science Center at San Antonio, and has been the Chief of Emergency Medicine at UT Medical Branch and at UTHSCSA with over 250 publications.

Originally described in approximately 30% of patients with type 1 diabetes mellitus, limited joint mobility occurs in 50% of patients older than age 10 years who have had diabetes for longer than 5 years. The condition restricts joint extension, making it difficult to press the hands flat against each other. The skin of patients with severe joint involvement has a thickened and waxy appearance.
Exposure to certain viral infections (mumps and Coxsackie viruses) or other environmental toxins may serve to trigger abnormal antibody responses that cause damage to the pancreas cells where insulin is made. Some of the antibodies seen in type 1 diabetes include anti-islet cell antibodies, anti-insulin antibodies and anti-glutamic decarboxylase antibodies. These antibodies can be detected in the majority of patients, and may help determine which individuals are at risk for developing type 1 diabetes.
About 40% of diabetes sufferers require oral agents for satisfactory blood glucose control, and some 40% need insulin injections. This hormone was isolated by Frederic Banting and Charles Best in 1921 in Canada. It revolutionized the treatment of diabetes and prevention of its complications, transforming Type 1 diabetes from a fatal disease to one in which long-term survival became achievable.
There are two main kinds of diabetes: type 1 diabetes and type 2 diabetes. More than 90% of all people with diabetes have type 2. Overall, more than 3 million Canadians have diabetes, and the number is rapidly rising. Over a third of people with type 2 diabetes are unaware they have the disease and are not receiving the required treatment because, for many people, early symptoms are not noticeable without testing.
The American Diabetes Association sponsored an international panel in 1995 to review the literature and recommend updates of the classification of diabetes mellitus. The definitions and descriptions that follow are drawn from the Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. The report was first approved in 1997 and modified in 1999. Although other terms are found in older literature and remain in use, their use in current clinical practice is inappropriate. Epidemiologic and research studies are facilitated by use of a common language.
The beta cells may be another place where gene-environment interactions come into play, as suggested by the previously mentioned studies that link beta cell genes with type 2. "Only a fraction of people with insulin resistance go on to develop type 2 diabetes," says Shulman. If beta cells can produce enough insulin to overcome insulin resistance, a factor that may be genetically predetermined, then a person can stay free of diabetes. But if the beta cells don't have good genes propping them up, then diabetes is the more likely outcome in a person with substantial 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.)
There is evidence that certain emotions can promote type 2 diabetes. A recent study found that depression seems to predispose people to diabetes. Other research has tied emotional stress to diabetes, though the link hasn't been proved. Researchers speculate that the emotional connection may have to do with the hormone cortisol, which floods the body during periods of stress. Cortisol sends glucose to the blood, where it can fuel a fight-or-flight response, but overuse of this system may lead to dysfunction.
Glycated hemoglobin (A1C) test. This blood test indicates your average blood sugar level for the past two to three months. It measures the percentage of blood sugar attached to hemoglobin, the oxygen-carrying protein in red blood cells. The higher your blood sugar levels, the more hemoglobin you'll have with sugar attached. An A1C level of 6.5 percent or higher on two separate tests indicates you have diabetes. A result between 5.7 and 6.4 percent is considered prediabetes, which indicates a high risk of developing diabetes. Normal levels are below 5.7 percent.
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
Diabetic ketoacidosis can be caused by infections, stress, or trauma, all of which may increase insulin requirements. In addition, missing doses of insulin is also an obvious risk factor for developing diabetic ketoacidosis. Urgent treatment of diabetic ketoacidosis involves the intravenous administration of fluid, electrolytes, and insulin, usually in a hospital intensive care unit. Dehydration can be very severe, and it is not unusual to need to replace 6-7 liters of fluid when a person presents in diabetic ketoacidosis. Antibiotics are given for infections. With treatment, abnormal blood sugar levels, ketone production, acidosis, and dehydration can be reversed rapidly, and patients can recover remarkably well.

How to prevent type 2 diabetes: Six useful steps What are the risks factors for developing type 2 diabetes, and how can we prevent it? Some factors such as blood sugar levels, body weight, fiber intake, and stress can be controlled to some extent, but others, such as age and family history cannot. Find out more about reducing the risk of developing this condition. Read now


The levels of glucose in the blood vary normally throughout the day. They rise after a meal and return to pre-meal levels within about 2 hours after eating. Once the levels of glucose in the blood return to premeal levels, insulin production decreases. The variation in blood glucose levels is usually within a narrow range, about 70 to 110 milligrams per deciliter (mg/dL) of blood in healthy people. If people eat a large amount of carbohydrates, the levels may increase more. People older than 65 years tend to have slightly higher levels, especially after eating.


Some people who have type 2 diabetes can achieve their target blood sugar levels with diet and exercise alone, but many also need diabetes medications or insulin therapy. The decision about which medications are best depends on many factors, including your blood sugar level and any other health problems you have. Your doctor might even combine drugs from different classes to help you control your blood sugar in several different ways.
central diabetes insipidus a metabolic disorder due to injury of the neurohypophyseal system, which results in a deficient quantity of antidiuretic hormone (ADH or vasopressin) being released or produced, resulting in failure of tubular reabsorption of water in the kidney. As a consequence, there is the passage of a large amount of urine having a low specific gravity, and great thirst; it is often attended by voracious appetite, loss of strength, and emaciation. Diabetes insipidus may be acquired through infection, neoplasm, trauma, or radiation injuries to the posterior lobe of the pituitary gland or it may be inherited or idiopathic.

When you have diabetes, excess sugar (glucose) builds up in your blood. Your kidneys are forced to work overtime to filter and absorb the excess sugar. If your kidneys can't keep up, the excess sugar is excreted into your urine, dragging along fluids from your tissues. This triggers more frequent urination, which may leave you dehydrated. As you drink more fluids to quench your thirst, you'll urinate even more.
If sugars in general are not associated with increased diabetes risk, but sodas are, it suggests the possibility that something other than sugar explains this relationship.16 Sodas are often accompanied by cheeseburgers, chicken nuggets, and other unhealthful foods. That is, soda consumption can be a sign of a diet focusing on fast foods or an overall unhealthful diet and lifestyle. And sugary snack foods (e.g., cookies and snack pastries) are often high in fat; the sugar lures us in to the fat calories hiding inside. Some, but not all, observational trials have sought to control for these confounding variables. 
Because both yeast and bacteria multiply more quickly when blood sugar levels are elevated, women with diabetes are overall at a higher risk of feminine health issues, such as bacterial infections, yeast infections, and vaginal thrush, especially when blood sugar isn't well controlled. And a lack of awareness about having prediabetes or diabetes can make managing blood sugar impossible.
×