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.
To understand why insulin is important, it helps to know more about how the body uses food for energy. Your body is made up of millions of cells. To make energy, these cells need food in a very simple form. When you eat or drink, much of the food is broken down into a simple sugar called "glucose." Then, glucose is transported through the bloodstream to these cells where it can be used to provide the energy the body needs for daily activities.
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.
10. Importance of keeping appointments and staying in touch with a health care provider for consultation and assessment. Periodic evaluation of the binding of glucose to hemoglobin (glycosylated hemoglobin or hemoglobin A1C testing) can give information about the effectiveness of the prescribed regimen and whether any changes need to be made. The ADA position statement on tests of glycemia in diabetes recommends routine testing for all patients with diabetes. It should be a part of the initial assessment of the patient, with subsequent measurements every three months to determine if the patient's metabolic control has been reached and maintained.
The protocol for therapy is determined by the type of diabetes; patients with either type 1 or type 2 must pay attention to their diet and exercise regimens. Insulin therapy may be prescribed for patients with type 2 diabetes as well as any who are dependent on insulin. In most cases, the type 2 diabetes patient can be treated effectively by reducing caloric intake, maintaining target weight, and promoting physical exercise.
While many experts believe that most type 1 genes have been identified, the situation with type 2 diabetes is much different. A recent study found that the known genetic links to type 2 probably account for only about 6 percent of the genetic predisposition for that form of diabetes. This could mean either that some of the genes discovered have a bigger effect than is currently believed or that "we are still missing 94 percent of the genes," says Atul Butte, MD, PhD, an assistant professor of pediatrics at Stanford University.
In patients with type 2 diabetes, stress, infection, and medications (such as corticosteroids) can also lead to severely elevated blood sugar levels. Accompanied by dehydration, severe blood sugar elevation in patients with type 2 diabetes can lead to an increase in blood osmolality (hyperosmolar state). This condition can worsen and lead to coma (hyperosmolar coma). A hyperosmolar coma usually occurs in elderly patients with type 2 diabetes. Like diabetic ketoacidosis, a hyperosmolar coma is a medical emergency. Immediate treatment with intravenous fluid and insulin is important in reversing the hyperosmolar state. Unlike patients with type 1 diabetes, patients with type 2 diabetes do not generally develop ketoacidosis solely on the basis of their diabetes. Since in general, type 2 diabetes occurs in an older population, concomitant medical conditions are more likely to be present, and these patients may actually be sicker overall. The complication and death rates from hyperosmolar coma is thus higher than in diabetic ketoacidosis.
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.
FIGURE 19-1 ■. This figure shows the hyperbolic relationship of insulin resistance and beta cell function. On the y-axis is beta cell function as reflected in the first-phase insulin response during intravenous (IV) glucose infusion; on the x-axis is insulin sensitivity and its mirror image resistance. In a subject with normal glucose tolerance (NGT) and beta-cell reserve, an increase in insulin resistance results in increased insulin release and normal glucose tolerance. In an individual for whom the capacity to increase insulin release is compromised, increasing insulin resistance with partial or no beta-cell compensation results in progression from normal glucose tolerance, to impaired glucose tolerance (IGT), and finally to diabetes (T2D). Differences between these categories are small at high insulin sensitivity, which may be maintained by weight reduction, exercise, and certain drugs. At a critical degree of insulin resistance, due to obesity or other listed factors, only a further small increment in resistance requires a large increase in insulin output. Those that can increase insulin secretion to this extent retain normal glucose tolerance; those who cannot achieve this degree of insulin secretion (e.g., due to a mild defect in genes regulating insulin synthesis, insulin secretion, insulin action, or an ongoing immune destruction of beta cells) now unmask varying degrees of carbohydrate intolerance. The product of insulin sensitivity (the reciprocal of insulin resistance) and acute insulin response (a measurement beta-cell function) has been called the “disposition index.” This index remains constant in an individual with normal beta cell compensation in response to changes in insulin resistance. IGT, impaired glucose tolerance; NGT, normal glucose tolerance; T2D, type 2 diabetes.
Rates of type 2 diabetes have increased markedly since 1960 in parallel with obesity. As of 2015 there were approximately 392 million people diagnosed with the disease compared to around 30 million in 1985. Typically it begins in middle or older age, although rates of type 2 diabetes are increasing in young people. Type 2 diabetes is associated with a ten-year-shorter life expectancy. Diabetes was one of the first diseases described. The importance of insulin in the disease was determined in the 1920s.
Your doctor will carefully examine you at each visit for diabetes. In particular they will examine your cardiovascular system, eyes and neurological systems to detect any complications present. In the acute phase you may appear wasted and dehydrated. You may have difficulty breathing and have a sweet smell to your breath. In the later stages, your doctor will check your pulse, listen to your heart, measure your blood pressure (often lying and standing) and examine your limbs to detect any loss of sensation or ulcers.
Diabetes was one of the first diseases described, with an Egyptian manuscript from c. 1500 BCE mentioning "too great emptying of the urine". The Ebers papyrus includes a recommendation for a drink to be taken in such cases. The first described cases are believed to be of type 1 diabetes. Indian physicians around the same time identified the disease and classified it as madhumeha or "honey urine", noting the urine would attract ants.
No single environmental trigger has been identified as causing diabetes mellitus, however both infectious agents and dietary factors are thought to be important. Various viruses have been implicated in the development of type I DM. They may act by initiating or modifying the autoimmune process. In particular, the rubella virus and coxsackie viruses have been closely studied. In particular, congenital rubella infection has shown direct relationships with the development of type 1 diabetes mellitus. This is presumably due to the virus (or antibodies against it) damaging the beta cells of the pancreas. Some research has looked at dietary factors that may be associated with type 1 diabetes. In particular, cow’s milk proteins (such as bovine serum albumin) which may have some similarities to pancreatic islet cell markers may be able to trigger the autoimmune process. Other chemicals including nitrosamines have been identified as causes of diabetes mellitus in animal models, but not in humans.
^ Jump up to: a b c d Inzucchi, SE; Bergenstal, RM; Buse, JB; Diamant, M; Ferrannini, E; Nauck, M; Peters, AL; Tsapas, A; Wender, R; Matthews, DR (March 2015). "Management of hyperglycaemia in type 2 diabetes, 2015: a patient-centred approach. Update to a Position Statement of the American Diabetes Association and the European Association for the Study of Diabetes". Diabetologia. 58 (3): 429–42. doi:10.1007/s00125-014-3460-0. PMID 25583541.
Nerve damage (neuropathy). Excess sugar can injure the walls of the tiny blood vessels (capillaries) that nourish your nerves, especially in the legs. This can cause tingling, numbness, burning or pain that usually begins at the tips of the toes or fingers and gradually spreads upward. Poorly controlled blood sugar can eventually cause you to lose all sense of feeling in the affected limbs. Damage to the nerves that control digestion can cause problems with nausea, vomiting, diarrhea or constipation. For men, erectile dysfunction may be an issue.
Most cases (95%) of type 1 diabetes mellitus are the result of environmental factors interacting with a genetically susceptible person. This interaction leads to the development of autoimmune disease directed at the insulin-producing cells of the pancreatic islets of Langerhans. These cells are progressively destroyed, with insulin deficiency usually developing after the destruction of 90% of islet cells.
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.
Insulin is a hormone that — in people without diabetes — ferries glucose, or blood sugar, to cells for energy or to be stored for later use. In people with diabetes, cells are resistant to insulin; as a result of this insulin resistance, sugar accumulates in the blood. While eating sugar by itself does not cause insulin resistance, Grieger says, foods with sugar and fat can contribute to weight gain, thereby reducing insulin sensitivity in the body.
What are symptoms of type 2 diabetes in children? Type 2 diabetes is becoming increasingly common in children, and this is linked to a rise in obesity. However, the condition can be difficult to detect in children because it develops gradually. Symptoms, treatment, and prevention of type 2 diabetes are similar in children and adults. Learn more here. Read now