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.
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.
Type 2 diabetes is a preventable disease that affects more than 9 percent of the U.S. population, or about 29 million people. According to the Centers for Disease Control and Prevention, more than a quarter — some 8 million people — remain undiagnosed. With complications including nerve damage, kidney damage, poor blood circulation, and even death, it’s important for us all to know the early signs of type 2 diabetes.
People with type 1 diabetes and certain people with type 2 diabetes may use carbohydrate counting or the carbohydrate exchange system to match their insulin dose to the carbohydrate content of their meal. "Counting" the amount of carbohydrate in a meal is used to calculate the amount of insulin the person takes before eating. However, the carbohydrate-to-insulin ratio (the amount of insulin taken for each gram of carbohydrate in the meal) varies for each person, and people with diabetes need to work closely with a dietician who has experience in working with people with diabetes to master the technique. Some experts have advised use of the glycemic index (a measure of the impact of an ingested carbohydrate-containing food on the blood glucose level) to delineate between rapid and slowly metabolized carbohydrates, although there is little evidence to support this approach.
To diagnose diabetes, doctors will take a medical history (ask you about symptoms) and ask for blood and urine samples. Finding protein and sugar in the urine are signs of type 2 diabetes. Increased glucose and triglyceride (a type of lipid or fat) levels in the blood are also common findings. In most cases, blood glucose levels are checked after a person has been fasting for 8 hours.
Type 2 diabetes, the most common type of diabetes, is a disease that occurs when your blood glucose, also called blood sugar, is too high. Blood glucose is your main source of energy and comes mainly from the food you eat. Insulin, a hormone made by the pancreas, helps glucose get into your cells to be used for energy. In type 2 diabetes, your body doesn’t make enough insulin or doesn’t use insulin well. Too much glucose then stays in your blood, and not enough reaches your cells.
Dr. Balentine received his undergraduate degree from McDaniel College in Westminster, Maryland. He attended medical school at the Philadelphia College of Osteopathic Medicine graduating in1983. He completed his internship at St. Joseph's Hospital in Philadelphia and his Emergency Medicine residency at Lincoln Medical and Mental Health Center in the Bronx, where he served as chief resident.
Oral Agents. Oral antidiabetic drugs (see hypoglycemic agents) are sometimes prescribed for patients with type 2 diabetes who cannot control their blood glucose with diet and exercise. These are not oral forms of insulin; they are sulfonylureas, chemically related to the sulfonamide antibiotics. Patients receiving them should be taught that the drug they are taking does not eliminate the need for a diet and exercise program. Only the prescribed dosage should be taken; it should never be increased to make up for dietary indiscretions or discontinued unless authorized by the physician.
Supporting evidence for Shulman's theory comes from observations about a rare genetic illness called lipodystrophy. People with lipodystrophy can't make fat tissue, which is where fat should properly be stored. These thin people also develop severe insulin resistance and type 2 diabetes. "They have fat stored in places it doesn't belong," like the liver and muscles, says Shulman. "When we treat them . . . we melt the fat away, reversing insulin resistance and type 2 diabetes." Shulman's theory also suggests why some people who carry extra fat don't get type 2. "There are some individuals who store fat [under the skin] who have relatively normal insulin sensitivity, a so-called fit fat individual," he says. Because of the way their bodies store fat, he believes, they don't get diabetes.
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
How does high blood sugar (hyperglycemia) feel? To maintain the right amount of blood sugar, the body needs insulin, a hormone that delivers this sugar to the cells. When insulin is lacking, blood sugar builds up. We describe symptoms of high blood sugar, including fatigue, weight loss, and frequent urination. Learn who is at risk and when to see a doctor here. Read now
The diabetic patient should learn to recognize symptoms of low blood sugar (such as confusion, sweats, and palpitations) and high blood sugar (such as, polyuria and polydipsia). When either condition results in hospitalization, vital signs, weight, fluid intake, urine output, and caloric intake are accurately documented. Serum glucose and urine ketone levels are evaluated. Chronic management of DM is also based on periodic measurement of glycosylated hemoglobin levels (HbA1c). Elevated levels of HbA1c suggest poor long-term glucose control. The effects of diabetes on other body systems (such as cerebrovascular, coronary artery, and peripheral vascular) should be regularly assessed. Patients should be evaluated regularly for retinal disease and visual impairment and peripheral and autonomic nervous system abnormalities, e.g., loss of sensation in the feet. The patient is observed for signs and symptoms of diabetic neuropathy, e.g., numbness or pain in the hands and feet, decreased vibratory sense, footdrop, and neurogenic bladder. The urine is checked for microalbumin or overt protein losses, an early indication of nephropathy. The combination of peripheral neuropathy and peripheral arterial disease results in changes in the skin and microvasculature that lead to ulcer formation on the feet and lower legs with poor healing. Approx. 45,000 lower-extremity diabetic amputations are performed in the U.S. each year. Many amputees have a second amputation within five years. Most of these amputations are preventable with regular foot care and examinations. Diabetic patients and their providers should look for changes in sensation to touch and vibration, the integrity of pulses, capillary refill, and the skin. All injuries, cuts, and blisters should be treated promptly. The patient should avoid constricting hose, slippers, shoes, and bed linens or walking barefoot. The patient with ulcerated or insensitive feet is referred to a podiatrist for continuing foot care and is warned that decreased sensation can mask injuries.
Hemoglobin A1c or HbA1c is a protein on the surface of red blood cells. The HbA1c test is used to monitor blood sugar levels in people with type 1 and type 2 diabetes over time. Normal HbA1c levels are 6% or less. HbA1c levels can be affected by insulin use, fasting, glucose intake (oral or IV), or a combination of these and other factors. High hemoglobin A1c levels in the blood increases the risk of microvascular complications, for example, diabetic neuropathy, eye, and kidney disease.
Beta cells are vulnerable to more than just bad genes, which may explain the associations between type 2 diabetes and environmental factors that aren't related to how much fat a body has or where it is stored. Beta cells carry vitamin D receptors on their surface, and people with vitamin D deficiency are at increased risk for type 2. Plus, several studies have shown that people with higher levels of toxic substances in their blood—such as from the PCBs found in fish fat—are at increased risk of type 2 diabetes, though a cause-and-effect relationship hasn't been proved. (Toxic substances and vitamin D have also been implicated in type 1 diabetes, but the disease mechanism may be unrelated to what's going on in type 2.)
As part of proper diabetes management, it is important to be aware of the symptoms of abnormal blood glucose levels and know how to properly monitor your blood glucose levels using a home glucose meter. You should remember to always keep glucose tablets or candies containing sugar with you at all times to manage low blood glucose levels (hypoglycemia). Symptoms of low blood glucose include:
People with full-blown type 2 diabetes are not able to use the hormone insulin properly, and have what’s called insulin resistance. Insulin is necessary for glucose, or sugar, to get from your blood into your cells to be used for energy. When there is not enough insulin — or when the hormone doesn’t function as it should — glucose accumulates in the blood instead of being used by the cells. This sugar accumulation may lead to the aforementioned complications.