Diabetes is a metabolic disorder that occurs when your blood sugar (glucose), is too high (hyperglycemia). Glucose is what the body uses for energy, and the pancreas produces a hormone called insulin that helps convert the glucose from the food you eat into energy. When the body does not produce enough insulin - or does not produce any at all - the glucose does not reach your cells to be used for energy. This results in diabetes.
With such a surplus of food nowadays, it's easy to overindulge without physical activity, leading to weight gain and, for some people, eventual Type 2 diabetes. "It's a lack of exercise and still eating like you're 20 years old," says Susan M. De Abate, a nurse and certified diabetes educator and team coordinator of the diabetes education program at Sentara Virginia Beach General Hospital.
Diabetes mellitus (DM) is best defined as a syndrome characterized by inappropriate fasting or postprandial hyperglycemia, caused by absolute or relative insulin deficiency and its metabolic consequences, which include disturbed metabolism of protein and fat. This syndrome results from a combination of deficiency of insulin secretion and its action. Diabetes mellitus occurs when the normal constant of the product of insulin secretion times insulin sensitivity, a parabolic function termed the “disposition index” (Figure 19-1), is inadequate to prevent hyperglycemia and its clinical consequences of polyuria, polydipsia, and weight loss. At high degrees of insulin sensitivity, small declines in the ability to secrete insulin cause only mild, clinically imperceptible defects in glucose metabolism. However, irrespective of insulin sensitivity, a minimum amount of insulin is necessary for normal metabolism. Thus, near absolute deficiency of insulin must result in severe metabolic disturbance as occurs in type 1 diabetes mellitus (T1DM). By contrast, with decreasing sensitivity to its action, higher amounts of insulin secretion are required for a normal disposition index. At a critical point in the disposition index curve (see Figure 19-1), a further small decrement in insulin sensitivity requires a large increase in insulin secretion; those who can mount these higher rates of insulin secretion retain normal glucose metabolism, whereas those who cannot increase their insulin secretion because of genetic or acquired defects now manifest clinical diabetes as occurs in type 2 diabetes (T2DM).
Hyperglycemic hyperosmolar nonketotic syndrome (HHNS). Signs and symptoms of this life-threatening condition include a blood sugar reading higher than 600 mg/dL (33.3 mmol/L), dry mouth, extreme thirst, fever greater than 101 F (38 C), drowsiness, confusion, vision loss, hallucinations and dark urine. Your blood sugar monitor may not be able to give you an exact reading at such high levels and may instead just read "high."
When you have diabetes, your body becomes less efficient at breaking food down into sugar, so you have more sugar sitting in your bloodstream, says Dobbins. “Your body gets rid of it by flushing it out in the urine.” So going to the bathroom a lot could be one of the diabetes symptoms you’re missing. Most patients aren’t necessarily aware of how often they use the bathroom, says Dr. Cypess. “When we ask about it, we often hear, ‘Oh yeah, I guess I’m going more often than I used to,’” he says. But one red flag is whether the need to urinate keeps you up at night. Once or twice might be normal, but if it’s affecting your ability to sleep, that could be a diabetes symptom to pay attention to. Make sure you know these diabetes myths that could sabotage your health.
Insulin is vital to patients with type 1 diabetes - they cannot live without a source of exogenous insulin. Without insulin, patients with type 1 diabetes develop severely elevated blood sugar levels. This leads to increased urine glucose, which in turn leads to excessive loss of fluid and electrolytes in the urine. Lack of insulin also causes the inability to store fat and protein along with breakdown of existing fat and protein stores. This dysregulation, results in the process of ketosis and the release of ketones into the blood. Ketones turn the blood acidic, a condition called diabetic ketoacidosis (DKA). Symptoms of diabetic ketoacidosis include nausea, vomiting, and abdominal pain. Without prompt medical treatment, patients with diabetic ketoacidosis can rapidly go into shock, coma, and even death may result.
Diabetes is a disease in which your blood glucose, or blood sugar, levels are too high. Glucose comes from the foods you eat. Insulin is a hormone that helps the glucose get into your cells to give them energy. With type 1 diabetes, your body does not make insulin. With type 2 diabetes, the more common type, your body does not make or use insulin well. Without enough insulin, the glucose stays in your blood.
Being too heavy gets the bulk of the blame for triggering type 2 diabetes. According to the National Institutes of Health, about 85 percent of people with type 2 diabetes are overweight or obese. But consider that the remaining 15 percent are not. Consider, too, that roughly two-thirds of overweight people and a third of those who are obese will never develop diabetes. In other words, normal-weight and thin people also develop type 2, while heavy people won't necessarily. Clearly, there is more to the connection between lifestyle and type 2 diabetes than just body size.
Rates of diabetes in 1985 were estimated at 30 million, increasing to 135 million in 1995 and 217 million in 2005. This increase is believed to be primarily due to the global population aging, a decrease in exercise, and increasing rates of obesity. 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. It is recognized as a global epidemic by the World Health Organization.
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.
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.
Type 1 diabetes mellitus is characterized by loss of the insulin-producing beta cells of the pancreatic islets, leading to insulin deficiency. This type can be further classified as immune-mediated or idiopathic. The majority of type 1 diabetes is of the immune-mediated nature, in which a T cell-mediated autoimmune attack leads to the loss of beta cells and thus insulin. It causes approximately 10% of diabetes mellitus cases in North America and Europe. Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Type 1 diabetes can affect children or adults, but was traditionally termed "juvenile diabetes" because a majority of these diabetes cases were found in children.
Insulin is needed to allow glucose to pass from the blood into most of the body cells. Only the cells of the brain and central nervous system can use glucose from the blood in the absence of insulin. Without insulin, most body cells metabolize substances other than glucose for energy. However, fat metabolism in the absence of glucose metabolism, creates ketone bodies which are poisonous and their build up is associated with hyperglycemic coma. In the absence of sufficient insulin, unmetabolized glucose builds up in the blood. Water is drawn from body cells by osmosis to dilute the highly concentrated blood, and is then excreted along with much of the glucose, once the renal threshold for glucose (usually 10 mmol/L) is exceeded. Dehydration follows.
Diabetic neuropathy is probably the most common complication of diabetes. Studies suggest that up to 50% of people with diabetes are affected to some degree. Major risk factors of this condition are the level and duration of elevated blood glucose. Neuropathy can lead to sensory loss and damage to the limbs. It is also a major cause of impotence in diabetic men.
There’s no cure for type 1 diabetes. People with type 1 diabetes don’t produce insulin, so it must be regularly injected into your body. Some people take injections into the soft tissue, such as the stomach, arm, or buttocks, several times per day. Other people use insulin pumps. Insulin pumps supply a steady amount of insulin into the body through a small tube.
Some people with type 2 diabetes are treated with insulin. Insulin is either injected with a syringe several times per day, or delivered via an insulin pump. The goal of insulin therapy is to mimic the way the pancreas would produce and distribute its own insulin, if it were able to manufacture it. Taking insulin does not mean you have done a bad job of trying to control your blood glucose—instead it simply means that your body doesn’t produce or use enough of it on its own to cover the foods you eat.
When you have type 2 diabetes, your cells don't get enough glucose, which may cause you to lose weight. Also, if you are urinating more frequently because of uncontrolled diabetes, you may lose more calories and water, resulting in weight loss, says Daniel Einhorn, MD, medical director of the Scripps Whittier Diabetes Institute and clinical professor of medicine at the University of California in San Diego.