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.
Before blood glucose levels rise, the body of a person destined for type 2 becomes resistant to insulin, much as bacteria can become resistant to antibiotics. Insulin is the signal for the muscles, fat, and liver to absorb glucose from the blood. As the body becomes resistant to insulin, the beta cells in the pancreas must pump out more of the hormone to compensate. People with beta cells that can't keep up with insulin resistance develop the high blood glucose of type 2 diabetes.
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. 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. Among those who are not obese, a high waist–hip ratio is often present. Smoking appears to increase the risk of type 2 diabetes mellitus.
It is a considerable challenge to obtain the goals of the intensively treated patients in the DCCT with the vast majority of people with diabetes given the more limited health care resources typically available in routine practice. If diabetes control can be improved without significant damage to quality of life, the economic, health, and quality of life savings associated with a reduction in complications in later life will be vast. Although some people who have had poorly controlled diabetes over many years do not develop complications, complications commonly arise after 15–20 years of diabetes and individuals in their 40s or even 30s may develop several complications in rapid succession. However, up until the early 1980s, patients had no way of monitoring their own blood glucose levels at home. Urine glucose monitoring only told them when their blood glucose had exceeded the renal threshold of approximately 10 mmol/L (i.e., was far too high), without being able to discriminate between the too high levels of 7–10 mmol/L or the hypoglycemic levels below 4 mmol/L. Clinics relied on random blood glucose testing and there were no measures of average blood glucose over a longer period. Since the 1980s there have been measures of glycosylated hemoglobin (GHb, HbA1, or HbA1c) which indicate average blood glucose over a six to eight week period and measures of glycosylated protein, fructosamine, which indicates average blood glucose over a two-week period. Blood-glucose meters for patients were first introduced in the early 1980s and the accuracy and convenience of the meters and the reagent strips they use has improved dramatically since early models. By the late 1990s blood-glucose monitoring is part of the daily routine for most people using insulin in developed countries. Blood-glucose monitoring is less often prescribed for tablet- and diet-alone-treated patients, financial reasons probably being allowed to outweigh the educational value of accurate feedback in improving control long term. The reduced risk of hypoglycemia and diabetic ketoacidosis in NIDDM patients not using insulin means that acute crises rarely arise in these patients though their risk of long-term complications is at least as great as in IDDM and might be expected to be reduced if feedback from blood-glucose monitoring were provided.
John P. Cunha, DO, is a U.S. board-certified Emergency Medicine Physician. Dr. Cunha's educational background includes a BS in Biology from Rutgers, the State University of New Jersey, and a DO from the Kansas City University of Medicine and Biosciences in Kansas City, MO. He completed residency training in Emergency Medicine at Newark Beth Israel Medical Center in Newark, New Jersey.
a complex disorder of carbohydrate, fat, and protein metabolism that is primarily a result of a deficiency or complete lack of insulin secretion by the beta cells of the pancreas or resistance to insulin. The disease is often familial but may be acquired, as in Cushing's syndrome, as a result of the administration of excessive glucocorticoid. The various forms of diabetes have been organized into categories developed by the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus of the American Diabetes Association. Type 1 diabetes mellitus in this classification scheme includes patients with diabetes caused by an autoimmune process, dependent on insulin to prevent ketosis. This group was previously called type I, insulin-dependent diabetes mellitus, juvenile-onset diabetes, brittle diabetes, or ketosis-prone diabetes. Patients with type 2 diabetes mellitus are those previously designated as having type II, non-insulin-dependent diabetes mellitus, maturity-onset diabetes, adult-onset diabetes, ketosis-resistant diabetes, or stable diabetes. Those with gestational diabetes mellitus are women in whom glucose intolerance develops during pregnancy. Other types of diabetes are associated with a pancreatic disease, hormonal changes, adverse effects of drugs, or genetic or other anomalies. A fourth subclass, the impaired glucose tolerance group, also called prediabetes, includes persons whose blood glucose levels are abnormal although not sufficiently above the normal range to be diagnosed as having diabetes. Approximately 95% of the 18 million diabetes patients in the United States are classified as type 2, and more than 70% of those patients are obese. About 1.3 million new cases of diabetes mellitus are diagnosed in the United States each year. Contributing factors to the development of diabetes are heredity; obesity; sedentary life-style; high-fat, low-fiber diets; hypertension; and aging. See also impaired glucose tolerance, potential abnormality of glucose tolerance, previous abnormality of glucose tolerance.
The 1989 "St. Vincent Declaration" was the result of international efforts to improve the care accorded to those with diabetes. Doing so is important not only in terms of quality of life and life expectancy but also economically – expenses due to diabetes have been shown to be a major drain on health – and productivity-related resources for healthcare systems and governments.
Intensive blood sugar lowering (HbA1c<6%) as opposed to standard blood sugar lowering (HbA1c of 7–7.9%) does not appear to change mortality. The goal of treatment is typically an HbA1c of 7 to 8% or a fasting glucose of less than 7.2 mmol/L (130 mg/dl); however these goals may be changed after professional clinical consultation, taking into account particular risks of hypoglycemia and life expectancy. Despite guidelines recommending that intensive blood sugar control be based on balancing immediate harms with long-term benefits, many people – for example people with a life expectancy of less than nine years who will not benefit, are over-treated.
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.
At the same time that the body is trying to get rid of glucose from the blood, the cells are starving for glucose and sending signals to the body to eat more food, thus making patients extremely hungry. To provide energy for the starving cells, the body also tries to convert fats and proteins to glucose. The breakdown of fats and proteins for energy causes acid compounds called ketones to form in the blood. Ketones also will be excreted in the urine. As ketones build up in the blood, a condition called ketoacidosis can occur. This condition can be life threatening if left untreated, leading to coma and death.
Type 2 diabetes: Type 2 diabetes affects the way the body uses insulin. While the body still makes insulin, unlike in type I, the cells in the body do not respond to it as effectively as they once did. This is the most common type of diabetes, according to the National Institute of Diabetes and Digestive and Kidney Diseases, and it has strong links with obesity.
The symptoms may relate to fluid loss and polyuria, but the course may also be insidious. Diabetic animals are more prone to infections. The long-term complications recognized in humans are much rarer in animals. The principles of treatment (weight loss, oral antidiabetics, subcutaneous insulin) and management of emergencies (e.g. ketoacidosis) are similar to those in humans.
Can you “exercise your way” out of this problem? Sometimes you can; however, the key is exercising properly. For younger patients, it is best to exercise briefly and intensely. Within the first 20 minutes of intense exercise, your body burns its sugar stores, which are hanging out in liver and muscle again. After that, you start burning fat. Although this sounds good; and to some extent it is, if you spend hours running or exercising excessively, you train your body to burn fat efficiently, which subsequently lead to also training your body to store fat efficiently.
Although urine can also be tested for the presence of glucose, checking urine is not a good way to monitor treatment or adjust therapy. Urine testing can be misleading because the amount of glucose in the urine may not reflect the current level of glucose in the blood. Blood glucose levels can get very low or reasonably high without any change in the glucose levels in the urine.
Insulin is only recommended for individuals for type 2 diabetics when they have not been able to get blood sugars low enough to prevent complications through other means. To avoid insulin, those with this health condition should work very hard to follow a healthy eating plan that includes a lot of vegetables and lean proteins, exercise every day, and keep stress in perspective. They also should take their oral drugs regularly. It can be difficult to follow these recommendations and the help of your doctor, nutritionist, diabetes educator, health coach, or integrative medicine practitioner may be helpful. If you who want to avoid taking medicine, work with health professionals who are knowledgeable about lifestyle medicine, and can help you understand how to fit the changes into your life.
Of course, you’re exhausted every now and then. But ongoing fatigue is an important symptom to pay attention to; it might mean the food you’re eating for energy isn’t being broken down and used by cells as it’s supposed to. “You’re not getting the fuel your body needs,” says Dobbins. “You’re going to be tired and feel sluggish.” But in many cases of type 2 diabetes, your sugar levels can be elevated for awhile, so these diabetes symptoms could come on slowly.
In this health topic, we discuss hyperglycemic hyperosmolar nonketotic syndrome (HHNS), an extremely serious complication that can lead to diabetic coma and even death in type 2 diabetes. This serious condition occurs when the blood sugar gets too high and the body becomes severely dehydrated. To prevent HHNS and diabetic coma in type 2 diabetes, check your blood sugar regularly as recommended by your health care provider; check your blood sugar more frequently when you are sick, drink plenty of fluids, and watch for signs of dehydration.