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A complication of diabetes mellitus characterized by a need for more than 200 units of insulin per day to control hyperglycemia and ketosis. The cause is associated with insulin binding by high levels of antibody.
Definition
Insulin resistance is a condition in which cells, particularly those of muscle, fat, and liver tissue, display "resistance" to insulin by failing to take up and utilize glucose for energy and metabolism (insulin normally promotes take up and utilization of blood glucose from the blood stream). In its early stages, the condition is asymptomatic, but may develop into Type II Diabetes. Although there are several established risk factors, the underlying cause is unknown.
It has been estimated that 30 to 33 million Americans are insulin resistant, and the number appears to be increasing.
Description
Insulin resistance is initially asymptomatic, and in its early stages can be detected only by laboratory tests. These tests will show an abnormally high blood sugar (glucose) level, but not high enough to be considered prediabetic or diabetic. While the condition does not always lead to further problems, the majority of people who reach the pre-diabetic level go on to develop Type II Diabetes (formerly called Maturity Onset Diabetes.
Causes & Symptoms
The cause of insulin resistance is unknown, although the condition has been seen to run in families, indicating that there is a genetic association. Being overweight, and lack of exercise are also associated with insulin resistance, although the nature of the relationship is not clear. Risk factors for insulin resistance are:
In its mildest form, insulin resistance causes no symptoms, and is only recognizable on laboratory tests. In more severe cases, there may be dark patches on the back of the neck or even a dark ring around the neck. The dark patches are called Acanthosis nigricans and may also cause darkening of skin color in the elbows, knees, knuckles, and armpits.
There is a constellation of symptoms now called metabolic syndrome or insulin resistance syndrome that is linked to insulin resistance. This syndrome was formerly called syndrome X. Metabolic syndrome is defined by the National Cholesterol Education Program as the presence of any three of the following conditions:
Note that the numbers are those from an expert panel convened by the National Institutes of Health in 2001. Other panels of similarly qualified experts have given slightly different definitions.
Diagnosis
The only means of diagnosis for insulin resistance is laboratory tests. While there are several tests that may be performed, the two most common screening tests are the fasting blood sugar test and glucose tolerance test.
Fasting blood sugar measures the blood glucose level after a 12-hour fast (no food). A normal level, according to the United Sates National Institute of Diabetes and Digestive and Kidney Disease (NIDDK), should be below 100 mg/dL (milligrams of glucose in every deciliter of blood. A value in the n the 100 to 125 mg/dL range is considered evidence of insulin resistance, and is considered prediabetic. A value of 126 mg/dL is considered diabetic. (Blood sugar levels after a 12 hr fast are typically lower than this, and are controlled by pancreatic insulin secretion that transports blood glucose out of the blood and into the muscles, brain, organs, and other tissues.)
The glucose tolerance test is performed after the patient has had nothing but water for 10 to 16 hours. The patient has his blood drawn for a a baseline blood glucose level. Next, the patient drinks a special sweetened test drink that contains exactly 75 grams of glucose (pregnant women are normally given 100 grams of glucose.) Blood is drawn again at one-half hour and each of the next six hours to compare blood glucose levels and watch their pattern in response to the sweet drink. Normally the blood sugar levels is lower before the drink, rises quickly during the first few hours, and slowly drops again. In insulin resistance, the blood sugar level rises but stays abnormally high because it is resistant to being removed from blood into tissues by insulin. High blood sugar from food or the test glucose drink stimulates the pancreas to secrete insulin into the blood. However, in insulin resistance, the insulin is secreted but is only partially absorbed by the tissues. According to the National Diabetes Information Clearinghouse (NDIC) a normal level would be below 140 mg/dL 2 hours after the drink. If it is in the 140 to 199 mg/dL range 2 hours after drinking the solution, the diagnosis is impaired glucose tolerance (IGT) or prediabetes. A level of 200 or higher, if confirmed, represents a diagnosis of diabetes.
Treatment
Among the most important treatment modalities are diet and exercise, weight loss if obese, endocrine hormone correction if unbalanced. In 2001, the National Institutes of Health completed the Diabetes Prevention Program (DPP), a clinical trial designed to find the most effective ways of preventing type 2 diabetes in overweight people with prediabetes. The researchers found that lifestyle changes reduced the risk of diabetes by 58 percent. Also, many people with prediabetes showed a return to normal blood glucose levels.
According to the DDP results, a mere half hour of brisk walking or bicycling five days a week can significantly reduce the risk of developing type 2 diabetes. Patients should use diet and exercise to reduce their body mass index (BMI) to 25 or below.
Smoking has been associated with insulin resistance, as well as with some of the more severe problems associated with diabetes. Discontinuing smoking should be a top priority.
A healthful diet, in addition to assisting in weight loss, may reduce serum lipids and reduce some of the risk factors for diabetes. One study recommended the Mediterranean diet as being the most beneficial for people with insulin resistance. Diet improvements include reducing sweets, desserts and high glycemic meals; eating balanced meals that contain protein, complex carbohydrates, fiber, greens and healthy oils, eating at regular times, and avoiding excess junk food and sugar.
No complimentary or alternative therapies have been proven to cure insulin resistance. Although several herbal remedies have been traditionally used for treatment of diabetes, none have been adequately documented as effective. Among medicinal plants shown to help lower elevated blood sugar are the Asian bitter melon and the Navaho Optunia cactus. Such herbal bitters as dandelion root and yellow dock can improve digestive strength and sometimes help, though no herbal remedy alone "cures" insulin resistance or diabetes. Guar gum, glucomannan, and psyllium seed all have demonstrated some ability to lower blood sugar in insulin resistance or diabetes, but none have been shown to be reliably effective for use in treatment of humans.
Allopathic Treatment
Insulin resistance does not normally require drug therapy; however, some studies have shown that the drugs used to treat type 2 diabetes may delay development of diabetes. Two classes of drugs now used to treat diabetes act by increasing insulin sensitivity, the biguanides and the thiazolidinediones; the other drugs used to treat diabetes act in different ways.
Although drugs from both classes have been effective in treatment of insulin resistance, neither drug has been as effective as a regimen of diet and exercise. Both classes of drugs have the potential for very severe adverse effects. They are also not approved by the FDA for control of insulin resistance, although physicians may prescribe them for this use if the condition appears to be getting worse without drug therapy. In one study, oral hypoglycemic drugs of various mechanisms that help reduce elevated blood blood glucose reduced the rate of disease progression from insulin resistance to diabetes by about one-third over a three-year period.
Expected Results
In mild asymptomatic insulin resistance, proper treatment may lead to a complete reversal, with normalization of blood sugar.
Even if complete normalization is impossible, treatment will lead to control of the condition, and a significant reduction in its rate of progression to diabetes.
Prevention
In insulin resistance, prevention is even better than treatment. Maintaining a normal weight, eating a balanced diet, and keeping up a regular program of aerobic exercise are the best preventive measures.
Resources
Books
Beers, M. H., and R. Berkow, eds. The Merck Manual of Diagnosis and Therapy, 17th ed. Whitehouse Station, New Jersey: Merck and Co., 2004.
Blumenthal, M., ed. The Complete German Commission E Monographs. Austin, TX: American Botanical Council, 1999.
Blumenthal, M., ed. Herbal Medicine. Austin, TX: American Botanical Council, 2000.
Hart, C. R., and M. K. Grossman. The Insulin Resistance Diet. Chicago: Contemporary Books, 2001
Periodicals
Brame, L., S. Verma, T. Anderson, A. Lteif, and K. Mather. "Insulin resistance as a therapeutic target for improved endothelial function: metformin." Curr Drug Targets Cardiovasc Haematol Disord (March 2004): 53–63.
Camp, H. S. "Thiazolidinediones in diabetes: current status and future outlook." Curr Opin Investig Drugs (April 2003): 406–11.
Cargo, D. M. "Association between smoking, insulin resistance and beta-cell function in a North-Western First Nation." Diabet Med (February 2004): 188–93.
Dzien, A., C. Dzien-Bischinger, F. Hoppichler, and M. Lechleitner. "The metabolic syndrome as a link between smoking and cardiovascular disease." Diabetes Obes Metab (March 2004): 127–32.
Nelson, M. R. "Managing 'metabolic syndrome' and multiple risk factors." Aust Fam Physician (April 2004): 201–5. Osei, K, S. Rhinesmith, T. Gaillard, and D. Schuster. "Beneficial metabolic effects of chronic glipizide in obese African Americans with impaired glucose tolerance: implications for primary prevention of type 2 diabetes." Metabolism (April 2004): 414–22.
Scheen, J. "Current management strategies for coexisting diabetes mellitus and obesity." Drugs (2003): 1165–84.
Yamamoto, Y., I. Sogawa, A. Nishina, S. Saeki, N. Ichikawa, and S. Iibata. "Improved hypolipidemic effects of xanthan gum-galactomannan mixtures in rats." Biosci Biotechnol Biochem (October 2000): 2165–71.
Organizations
American Association of Clinical Endocrinologists (AACE). 1000 Riverside Avenue, Suite 205, Jacksonville, FL 32204.
National Organization for Rare Disorders. 55 Kenosia Avenue, PO Box 1968, Danbury, CT 06813-1968.
[Article by: Samuel Uretsky, Pharm.D.]
A decreased sensitivity of target cells (e.g. muscle fibres) to insulin. Insulin resistance is one cause of diabetes mellitus (Type II diabetes, which usually occurs in adulthood and develops gradually). Acute bouts of aerobic exercise improves the responsiveness of target cells to insulin, reducing the cells’ requirements and reducing the insulin dosages some diabetics require.
| eMedicine | med/1173 | |
|---|---|---|
| MeSH | C18.452.394.968.500 | |
Insulin resistance is the condition in which normal amounts of insulin are inadequate
to produce a normal insulin response from fat, muscle and
liver cells. Insulin resistance in fat cells results in
hydrolysis of stored triglycerides, which elevates free
fatty acids in the
In a person with normal metabolism, insulin is released from the beta (β) cells of the Islets of Langerhans located in the pancreas after eating ("postprandial"), and it signals insulin-sensitive tissues in the body (e.g., muscle, adipose) to absorb glucose to lower blood glucose to a normal level (approximately 5 mmol/L (mM), or 90 mg/dL). In an insulin-resistant person, normal levels of insulin do not trigger the signal for glucose absorption by muscle and adipose cells. To compensate for this, the pancreas in an insulin-resistant individual releases much more insulin such that the cells are adequately triggered to absorb glucose. On occasion, this can lead to a steep drop in blood sugar and a hypoglycemic reaction several hours after the meal.
The most common type of insulin resistance is associated with a disease state known as metabolic syndrome. Insulin resistance can progress to full type 2 diabetes. This is often seen when hyperglycemia develops after a meal, when pancreatic β-cells are unable to produce adequate insulin to maintain normal blood sugar levels (euglycemia). The inability of the β-cells to produce more insulin in a condition of hyperglycemia is what characterizes the transition from insulin resistance to type 2 diabetes.[1]
Various disease states make the body tissues more resistant to the actions of insulin. Examples include infection (mediated by the cytokine TNFα) and acidosis. Recent research is investigating the roles of adipokines (the cytokines produced by adipose tissue) in insulin resistance. Certain drugs may also be associated with insulin resistance (e.g., glucocorticoids).
Elevated blood levels of glucose regardless of cause leads to increased glycation of proteins.
Insulin resistance is often found in people with visceral adiposity (i.e., a high degree of fatty tissue underneath the abdominal muscle wall - as distinct from subcutaneous adiposity or fat between the skin and the muscle wall), hypertension, hyperglycemia and dyslipidemia involving elevated triglycerides, small dense low-density lipoprotein (sdLDL) particles, and decreased HDL cholesterol levels.
Insulin resistance is also often associated with a hypercoagulable state (impaired fibrinolysis) and increased inflammatory cytokine levels.
Insulin resistance is also occasionally found in patients who use insulin. In this case, the production of antibodies against insulin leads to lower-than-expected falls of glucose levels (glycemia) after a given dose of insulin. With the development of human insulin and analogues in the 1980s and the decline in the use of animal insulins (e.g., pork, beef), this type of insulin resistance has become very uncommon.
A fasting serum insulin level of greater than the upper limit of normal for the assay used (approximately 60pmol/L) is considered evidence of insulin resistance.
During a glucose tolerance test, which may be used to diagnose diabetes mellitus, a fasted patient takes a 75 gram oral dose of glucose. Blood glucose levels are then measured over the following 2 hours.
Interpretation is based on WHO guidelines. After 2 hours a Glycemia less than 7.8 mmol/L is considered normal, a glycaemia of between 7.8 to 11.0 is considered as Impaired Glucose Tolerance (IGT) and a glycaemia of greater than or equal to 11.1 is considered Diabetes Mellitus.
OGTT can be normal or mildly abnormal in simple insulin resistance. Often, there are raised glucose levels in the early measurements, reflecting the loss of a postprandial (after the meal) peak in insulin production. Extension of the testing (for several more hours) may reveal a hypoglycemic "dip," which is a result of an overshoot in insulin production after the failure of the physiologic postprandial insulin response.
Hyperinsulinemic euglycemic clamp
The gold standard for investigating and quantifying insulin resistance is the "hyperinsulinemic euglycemic clamp," so-called because it measures the amount of glucose necessary to compensate for an increased insulin level without causing hypoglycemia.[2] The test is rarely performed in clinical care, but is used in medical research, for example, to assess the effects of different medications. The rate of glucose infusion is commonly referred to in diabetes literature as the GINF value.
The procedure takes about 2 hours. Through a peripheral vein, insulin is infused at 10-120 mU per m2 per minute. In order to compensate for the insulin infusion, glucose 20% is infused to maintain blood sugar levels between 5 and 5.5 mmol/l. The rate of glucose infusion is determined by checking the blood sugar levels every 5 to 10 minutes. Low-dose insulin infusions are more useful for assessing the response of the liver, whereas high-dose insulin infusions are useful for assessing peripheral (i.e., muscle and fat) insulin action.
The rate of glucose infusion during the last 30 minutes of the test determines insulin sensitivity. If high levels (7.5 mg/min or higher) are required, the patient is insulin-sensitive. Very low levels (4.0 mg/min or lower) indicate that the body is resistant to insulin action. Levels between 4.0 and 7.5 mg/min are not definitive and suggest "impaired glucose tolerance," an early sign of insulin resistance.
This basic technique can be significantly enhanced by the use of glucose tracers. Glucose can be labeled with either stable or radioactive atoms. Commonly-used tracers are 3-3H glucose (radioactive), 6,6 2H-glucose (stable) and 1-13C Glucose (stable). Prior to beginning the hyperinsulinemic period, a 3h tracer infusion enables one to determine the basal rate of glucose production. During the clamp, the plasma tracer concentrations enable the calculation of whole-body insulin-stimulated glucose metabolism, as well as the production of glucose by the body (i.e., endogenous glucose production).
Modified Insulin Suppression Test
Another measure of insulin resistance is the modified insulin suppression test developed by Gerald Reaven at Stanford University. The test correlates well with the euglycemic clamp with less operator-dependent error. This test has been used to advance the large body of research relating to the metabolic syndrome.
Patients initially receive 25 mcg of octreotide (Sandostatin) in 5 ml of normal saline over 3 to 5 min IV as an initial bolus, and then will be infused continuously with an intravenous infusion of somatostatin (0.27microgm/m2/min) to suppress endogenous insulin and glucose secretion. Insulin and 20% glucose is then infused at rates of 32 and 267mg/m2/min, respectively. Blood glucose is checked at zero, 30, 60, 90, and 120 minutes, and then every 10 minutes for the last half-hour of the test. These last 4 values are averaged to determine the steady-state plasma glucose level. Subjects with an SSPG greater than 150mg/dl are considered to be insulin-resistant.
Given the complicated nature of the "clamp" technique (and the potential dangers of hypoglycemia in some patients), alternatives have been sought to simplify the measurement of insulin resistance. The first was the Homeostatic Model Assessment (HOMA), and a more recent method is the QUICKI (quantitative insulin sensitivity check index). Both employ fasting insulin and glucose levels to calculate insulin resistance, and both correlate reasonably with the results of clamping studies. Wallace et al point out that QUICKI is the logarithm of the value from one of the HOMA equations.[3]
The cause of the vast majority of cases of insulin resistance remains unknown. However, insulin resistance might be caused by a high-carbohydrate diet. Some physicians also believe that glucosamine (often prescribed for joint problems) may cause insulin resistance.
Several associated conditions include
Insulin resistance may also be caused by the damage of liver cells having undergone a defect of insulin receptors in hepatocytes.
The primary treatment for insulin resistance is exercise and weight loss. In some individuals, a low glycemic index or a
low-carbohydrate diet may also help. Fasting might also help. Both
The Diabetes Prevention Program showed that exercise and diet were nearly twice as effective as
Some types of Monounsaturated fatty acids and saturated fats appear to promote insulin resistance, whereas some types of polyunsaturated fatty acids (omega-3) can increase insulin sensitivity.[6][7][8]
There are scientific studies showing that chromium picolinate can increase insulin sensitivity, especially in type 2 diabetics, but other studies show no effect. The results are controversial.
Naturopathic approaches to insulin resistance have been advocated including supplementation of vanadium, bitter melon (momordica), and Gymnema sylvestre.[9]
The concept that insulin resistance may be the underlying cause of diabetes mellitus type 2 was first advanced by Sir Harold Percival Himsworth of the University College Hospital Medical Center in London in 1936.[10]
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