Schedule a yearly physical exam and regular eye exams. Your regular diabetes checkups aren't meant to replace regular physicals or routine eye exams. During the physical, your doctor will look for any diabetes-related complications, as well as screen for other medical problems. Your eye care specialist will check for signs of retinal damage, cataracts and glaucoma.
There is currently no cure for diabetes. The condition, however, can be managed so that patients can live a relatively normal life. Treatment of diabetes focuses on two goals: keeping blood glucose within normal range and preventing the development of long-term complications. Careful monitoring of diet, exercise, and blood glucose levels are as important as the use of insulin or oral medications in preventing complications of diabetes. In 2003, the American Diabetes Association updated its Standards of Care for the management of diabetes. These standards help manage health care providers in the most recent recommendations for diagnosis and treatment of the disease.

Lifestyle factors are important to the development of type 2 diabetes, including obesity and being overweight (defined by a body mass index of greater than 25), lack of physical activity, poor diet, stress, and urbanization.[10][30] Excess body fat is associated with 30% of cases in those of Chinese and Japanese descent, 60–80% of cases in those of European and African descent, and 100% of cases in Pima Indians and Pacific Islanders.[13] Among those who are not obese, a high waist–hip ratio is often present.[13] Smoking appears to increase the risk of type 2 diabetes mellitus.[31]


Dietary factors also influence the risk of developing type 2 diabetes. Consumption of sugar-sweetened drinks in excess is associated with an increased risk.[32][33] The type of fats in the diet are important, with saturated fats and trans fatty acids increasing the risk, and polyunsaturated and monounsaturated fat decreasing the risk.[26] Eating a lot of white rice appears to play a role in increasing risk.[34] A lack of exercise is believed to cause 7% of cases.[35] Persistent organic pollutants may play a role.[36]
Monitoring your caloric intake may be helpful if you’re overweight, but everyone with type 2 diabetes should track how many carbs they’re taking in. That can be tricky because carbs are in many of the common foods you may already eat, but there are both good and bad sources of carbs. Fruits and vegetables, for example, are good sources, while pretzels and cookies are bad sources. (29)
When you have Type 2 diabetes, you may start out with something called insulin resistance. This means your cells do not respond well to the insulin you are making. "Insulin levels may be quite high, especially in the early stages of the disease. Eventually, your pancreas may not be able to keep up, and insulin secretion goes down," Rettinger explains. Insulin resistance becomes more common as you put on more weight, especially weight around your belly.
People with type 2 diabetes have insulin resistance, which means the body cannot use insulin properly to help glucose get into the cells. In people with type 2 diabetes, insulin doesn’t work well in muscle, fat, and other tissues, so your pancreas (the organ that makes insulin) starts to put out a lot more of it to try and compensate. "This results in high insulin levels in the body,” says Fernando Ovalle, MD, director of the multidisciplinary diabetes clinic at the University of Alabama in Birmingham. This insulin level sends signals to the brain that your body is hungry.
Being overweight is a risk factor for developing diabetes, but other risk factors such as how much physical activity you get, family history, ethnicity, and age also play a role. Unfortunately, many people think that weight is the only risk factor for type 2 diabetes, but many people with type 2 diabetes are at a normal weight or only moderately overweight.

Diagnosis. The most common diagnostic tests for diabetes are chemical analyses of the blood such as the fasting plasma glucose. Capillary blood glucose monitoring can be used for screening large segments of the population. Portable equipment is available and only one drop of blood from the fingertip or earlobe is necessary. Capillary blood glucose levels have largely replaced analysis of the urine for glucose. Testing for urinary glucose can be problematic as the patient may have a high renal threshold, which would lead to a negative reading for urinary glucose when in fact the blood glucose level was high.
People with these risk factors should be screened for diabetes at least once every three years. Diabetes risk can be estimated using online risk calculators. Doctors may measure fasting blood glucose levels and hemoglobin A1C level, or do an oral glucose tolerance test. If the test results are on the border between normal and abnormal, doctors do the screening tests more often, at least once a year.
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.

Cardiovascular Medicine Book Dentistry Book Dermatology Book Emergency Medicine Book Endocrinology Book Gastroenterology Book Geriatric Medicine Book Gynecology Book Hematology and Oncology Book Human Immunodeficiency Virus Book Infectious Disease Book Jokes Book Mental Health Book Neonatology Book Nephrology Book Neurology Book Obstetrics Book Ophthalmology Book Orthopedics Book Otolaryngology Book Pathology and Laboratory Medicine Book Pediatrics Book Pharmacology Book Practice Management Book Prevention Book Pulmonology Book Radiology Book Rheumatology Book Sports Medicine Book Surgery Book Urology Book
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
n a metabolic disorder caused primarily by a defect in the production of insulin by the islet cells of the pancreas, resulting in an inability to use carbohydrates. Characterized by hyperglycemia, glycosuria, polyuria, hyperlipemia (caused by imperfect catabolism of fats), acidosis, ketonuria, and a lowered resistance to infection. Periodontal manifestations if blood sugar is not being controlled may include recurrent and multiple periodontal abscesses, osteoporotic changes in alveolar bone, fungating masses of granulation tissue protruding from periodontal pockets, a lowered resistance to infection, and delay in healing after periodontal therapy. See also blood glucose level(s).

A proper diet and exercise are the foundations of diabetic care,[23] with a greater amount of exercise yielding better results.[80] Exercise improves blood sugar control, decreases body fat content and decreases blood lipid levels, and these effects are evident even without weight loss.[81] Aerobic exercise leads to a decrease in HbA1c and improved insulin sensitivity.[82] Resistance training is also useful and the combination of both types of exercise may be most effective.[82]
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.
Type 2 DM begins with insulin resistance, a condition in which cells fail to respond to insulin properly.[2] As the disease progresses, a lack of insulin may also develop.[12] This form was previously referred to as "non insulin-dependent diabetes mellitus" (NIDDM) or "adult-onset diabetes".[2] The most common cause is excessive body weight and insufficient exercise.[2]
The good news is that prevention plays an important role in warding off these complications. By maintaining tight control of your blood glucose—and getting it as close to normal as possible—you’ll help your body function in the way that it would if you did not have diabetes. Tight control helps you decrease the chances that your body will experience complications from elevated glucose levels.
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.
×