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).


Oral glucose tolerance test (OGTT): With this test you will be required to fast for at least 8 hours and then are given a drink with 75 g of carbohydrate. Your blood glucose is checked at fasting and then 2 hours after drinking the solution. If your blood glucose is 11.1 mmol/L or higher, your doctor may diagnose diabetes. If your blood glucose 2 hours after drinking the solution is between 7.8 to 11.1 mmol/L, your doctor may diagnose prediabetes. This is the preferred method to test for gestational diabetes.
When the blood glucose level rises above 160 to 180 mg/dL, glucose spills into the urine. When the level of glucose in the urine rises even higher, the kidneys excrete additional water to dilute the large amount of glucose. Because the kidneys produce excessive urine, people with diabetes urinate large volumes frequently (polyuria). The excessive urination creates abnormal thirst (polydipsia). Because excessive calories are lost in the urine, people may lose weight. To compensate, people often feel excessively hungry.
Type 2 diabetes (T2D) is more common than type 1 diabetes with about 90 to 95 percent of people with diabetes having T2D. According to the Centers for Disease Control and Prevention’s report, 30.3 million Americans, or 9.4% of the US population have diabetes.1 More alarming, an estimated 84 million more American adults have prediabetes, which if not treated, will advance to diabetes within five years.1
Diabetes is a serious and costly disease which is becoming increasingly common, especially in developing countries and disadvantaged minorities. However, there are ways of preventing it and/or controlling its progress. Public and professional awareness of the risk factors for, and symptoms of diabetes are an important step towards its prevention and control.

Type 2 diabetes (T2D) is more common than type 1 diabetes with about 90 to 95 percent of people with diabetes having T2D. According to the Centers for Disease Control and Prevention’s report, 30.3 million Americans, or 9.4% of the US population have diabetes.1 More alarming, an estimated 84 million more American adults have prediabetes, which if not treated, will advance to diabetes within five years.1

To treat diabetic retinopathy, a laser is used to destroy and prevent the recurrence of the development of these small aneurysms and brittle blood vessels. Approximately 50% of patients with diabetes will develop some degree of diabetic retinopathy after 10 years of diabetes, and 80% retinopathy after 15 years of the disease. Poor control of blood sugar and blood pressure further aggravates eye disease in diabetes.


Hypoglycemic reactions are promptly treated by giving carbohydrates (orange juice, hard candy, honey, or any sugary food); if necessary, subcutaneous or intramuscular glucagon or intravenous dextrose (if the patient is not conscious) is administered. Hyperglycemic crises are treated initially with prescribed intravenous fluids and insulin and later with potassium replacement based on laboratory values.
Treatment of high blood pressure and high cholesterol levels, which can contribute to circulation problems, can help prevent some of the complications of diabetes as well. A low dose of aspirin taken daily is recommended in people with risk factors for heart disease. All people with diabetes who are between 40 and 75 years are given a statin (a drug to decrease cholesterol levels) regardless of cholesterol levels. Younger people with an elevated risk of heart disease should also take a statin .

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).


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.

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.
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.
Type 1 DM is caused by autoimmune destruction of the insulin-secreting beta cells of the pancreas. The loss of these cells results in nearly complete insulin deficiency; without exogenous insulin, type 1 DM is rapidly fatal. Type 2 DM results partly from a decreased sensitivity of muscle cells to insulin-mediated glucose uptake and partly from a relative decrease in pancreatic insulin secretion.
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.
Accelerated atherosclerosis is the main underlying factor contributing to the high risk of atherothrombotic events in DM patients. CAD, peripheral vascular disease, stroke, and increased intima-media thickness are the main macrovascular complications. Diabetics are 2–4 times more likely to develop stroke than people without DM.2 CVD, particularly CAD, is the leading cause of morbidity and mortality in patients with DM.4 Patients with T2DM have a 2- to 4-fold increase in the risk of CAD, and patients with DM but without previous myocardial infarction (MI) carry the same level of risk for subsequent acute coronary events as nondiabetic patients with previous MI.5 Furthermore, people with diabetes have a poorer long-term prognosis after MI, including an increased risk for congestive heart failure and death.
One particular type of sugar that has attracted a lot of negative attention is high-fructose corn syrup (HFCS) — and for good reason, as multiple studies suggest HFCS can influence diabetes risk. Some research in people who are overweight and obese, for example, suggests regularly consuming drinks sweetened with either fructose, a byproduct of HFCS, or glucose can lead to weight gain, and drinks with fructose in particular may reduce insulin sensitivity and spike blood sugar levels.
While poor vision is hardly uncommon—more than 60 percent of the American population wears glasses or contacts, after all—sudden changes in your vision, especially blurriness, need to be addressed by your doctor. Blurry vision is often a symptom of diabetes, as high blood sugar levels can cause swelling in the lenses of your eye, distorting your sight in the process. Fortunately, for many people, the effect is temporary and goes away when their blood sugar is being managed.

Some patients with type 2 DM can control their disease with a calorically restricted diet (for instance 1600 to 1800 cal/day), regular aerobic exercise, and weight loss. Most patients, however, require the addition of some form of oral hypoglycemic drug or insulin. Oral agents to control DM include sulfonylurea drugs (such as glipizide), which increase pancreatic secretion of insulin; biguanides or thiazolidinediones (such as metformin or pioglitazone), which increase cellular sensitivity to insulin; or a-glucosidase inhibitors (such as acarbose), which decrease the absorption of carbohydrates from the gastrointestinal tract. Both types of diabetics also may be prescribed pramlintide (Symlin), a synthetic analog of human amylin, a hormone manufactured in the pancreatic beta cells. It enhances postprandial glucose control by slowing gastric emptying, decreasing postprandial glucagon concentrations, and regulating appetite and food intake; thus pramlintide is helpful for patients who do not achieve optimal glucose control with insulin and/or oral antidiabetic agents. When combinations of these agents fail to normalize blood glucose levels, insulin injections are added. Tight glucose control can reduce the patient’s risk of many of the complications of the disease. See: illustration

Type 1 diabetes in pediatric patients has been linked to changes in cognition and brain structure, with a study by Siller et al finding lower volume in the left temporal-parietal-occipital cortex in young patients with type 1 diabetes than in controls. The study also indicated that in pediatric patients, higher severity of type 1 diabetes presentation correlates with greater structural differences in the brain at about 3 months following diagnosis. The investigators found that among study patients with type 1 diabetes, an association existed between the presence of diabetic ketoacidosis at presentation and reduced radial, axial, and mean diffusivity in the major white matter tracts on magnetic resonance imaging (MRI). In those with higher glycated hemoglobin (HbA1c) levels, hippocampal, thalamic, and cerebellar white matter volumes were lower, as was right posterior parietal cortical thickness, while right occipital cortical thickness was greater. Patients in the study were aged 7-17 years. [43]

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Although many of the symptoms of type 1 and type 2 diabetes are similar, they present in very different ways. Many people with type 2 diabetes won’t have symptoms for many years. Then often the symptoms of type 2 diabetes develop slowly over the course of time. Some people with type 2 diabetes have no symptoms at all and don’t discover their condition until complications develop.
A growing number of people in the U.S. and throughout the world are overweight and more prone to develop Type 2 diabetes, particularly if they have the genetics for it. "Type 2 diabetes can be caused by genetic inheritance, but by far the obesity epidemic has created massive increases in the occurrence of Type 2 diabetes. This is due to the major insulin resistance that is created by obesity," Gage says.
Diabetes mellitus, or simply diabetes, is a group of diseases in which a person does not produce enough insulin, or because it does not respond to the insulin that is produced. Insulin is a hormone that controls the amount of glucose (sugar) in the blood. Diabetes leads to high blood sugar levels, which can lead to damage of blood vessels, organs, and nerves.
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.
Impaired glucose tolerance (IGT) and impaired fasting glycaemia (IFG) refer to levels of blood glucose concentration above the normal range, but below those which are diagnostic for diabetes. Subjects with IGT and/or IFG are at substantially higher risk of developing diabetes and cardiovascular disease than those with normal glucose tolerance. The benefits of clinical intervention in subjects with moderate glucose intolerance is a topic of much current interest.
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
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