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eMedicine Specialties > Endocrinology > Metabolic Disorders
Insulin Resistance
Author: Samuel T Olatunbosun, MD, FACP, Chief, Internal Medicine, 56th Medical Group, Luke Air Force Base
Coauthor(s): Samuel Dagogo-Jack, MD, MBBS, MSc, FRCP, Professor of Medicine, Program Director, Division of Endocrinology, Diabetes and Metabolism, University of Tennessee Health Science Center
Contributor Information and Disclosures
Updated: Apr 16, 2010
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Overview
Differential Diagnoses & Workup
Treatment & Medication
Follow-up
References
Keywords
Further Reading
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Background
Insulin resistance is a state in which a given concentration of insulin produces a less-than-expected biological effect. Insulin resistance has also been arbitrarily defined as the requirement of 200 or more units of insulin per day to attain glycemic control and to prevent ketosis.
The syndromes of insulin resistance actually make up a broad clinical spectrum, which includes obesity, glucose intolerance, diabetes, and the metabolic syndrome, as well as an extreme insulin-resistant state. Many of these disorders are associated with various endocrine, metabolic, and genetic conditions. These syndromes may also be associated with immunological diseases and may exhibit distinct phenotypic characteristics.
The metabolic syndrome —a state of insulin-resistance that is also known as either syndrome X or the dysmetabolic syndrome—has drawn the greatest attention because of its public health importance.
In an effort to clinically identify patients with insulin resistance, various organizations have developed diagnostic criteria. The most commonly used criteria in the United States are those of the National Cholesterol Education Program/Adult Treatment Panel III (NCEP/ATP III).
•NCEP/ATP III criteria for the diagnosis of the metabolic syndrome include the following (diagnosis is made when 3 or more are present):
◦Waist circumference of more than 102 cm in men or more than 88 cm in women
◦Fasting triglyceride level of 150 mg/dL or higher
◦Blood pressure level of 130/85 mm Hg or higher
◦High-density lipoprotein cholesterol (HDL-C) level of less than 40 mg/dL in men or less than 50 mg/dL in women
◦Fasting glucose level of 110 mg/dL or higher (which has been changed to 100 mg/dL to reflect revised criteria for impaired fasting glucose [IFG])
•The World Health Organization (WHO) criteria for the diagnosis of the metabolic syndrome include the following:
◦Type 2 diabetes
◦IFG level of 101-125 mg/dL
◦Impaired glucose tolerance (IGT) (glucose level of 140-199 mg/dL 2 h after administration of 75 g of glucose)
◦Glucose uptake level of less than the lowest quartile for ethnic population under hyperinsulinemic, euglycemic conditions if the fasting glucose level is normal
◦In addition to the aforementioned criteria, the diagnosis must also include 2 of the following:
■Use of antihypertensive medication; blood pressure of 140 mm Hg systolic or higher, 90 mm Hg diastolic or higher, or both
■Triglyceride level of 150 mg/dL or higher
■HDL-C level of less than 35 mg/dL in men or less than 39 mg/dL in women
■Body mass index (BMI) of more than 30 kg/m2, waist-to-hip ratio of more than 0.9 in men or more than 0.85 in women, or both
■Urinary albumin excretion level of 20 mcg/min or higher or albumin-creatinine ratio of 30 mg/g or higher
•The American Association of Clinical Endocrinologists (AACE) clinical criteria for diagnosis of insulin resistance syndrome include the following:
◦BMI of 25 kg/m2 or higher
◦Triglyceride level of 150 mg/dL or higher
◦HDL-C level of less than 40 mg/dL in men or less than 50 mg/dL in women
◦Blood pressure of 130/85 mm Hg or higher
◦Glucose level of more than 140 mg/dL 2 hours after administration of 75 g of glucose
◦Fasting glucose level of 110-126 mg/dL
◦Additional risk factors include the following:
■Family history of type 2 diabetes
■Hypertension
■Coronary heart disease (CHD)1 ■Polycystic ovary syndrome (PCOS)2 ■Sedentary lifestyle
■Advanced age
■Ethnic groups at high risk for type 2 diabetes or for CHD
The ATP III criteria use fasting glucose level as the only measurement of glucose tolerance, while the WHO and AACE criteria include the option of performing a 2-hour oral glucose tolerance test (OGTT). The OGTT better identifies individuals at risk for endothelial damage due to hyperglycemia, because IGT has been shown to be independently associated with endothelial dysfunction and, hence, cardiovascular risk.1
In a global consensus statement, an International Diabetes Federation (IDF) panel presented a worldwide definition of the metabolic syndrome aimed at facilitating early detection and more intensive management of the condition, with the hope of reducing the long-term risk of cardiovascular disease (CVD) and diabetes.
•According to the definition by the IDF panel, the diagnostic criteria for the metabolic syndrome include central obesity (defined as waist circumference >94 cm in men or >80 cm in women in Europid persons and in ethnic-specific levels in Chinese, Japanese, and South Asian persons) together with 2 of the following:
◦Triglyceride level of 1.7 mmol/L (150 mg/dL) or higher
◦Low HDL-C level (defined as <1.04 mmol/L [40 mg/dL] in men or <1.29 mmol/L [50 mg/dL] in women)
◦Blood pressure of 130/85 mm Hg or higher
◦Fasting hyperglycemia (defined as glucose level >5.6 mmol/L [100 mg/dL]) or previous diagnosis of diabetes or IGT.
The scientific basis for the definition of the metabolic syndrome and its clinical utility have been debated. The debate was accentuated by a joint statement from the American Diabetes Association and the European Association for the Study of Diabetes. However, both sides of this debate generally agree that the risk factors commonly coexist in the same patient and that insulin resistance is the major underlying mechanism. Moreover, the metabolic syndrome serves as a clinical tool to raise awareness among health care providers, thus assisting in identifying high-risk individuals.
Recent studies
Uruska et al investigated a possible association between insulin resistance and microangiopathy in patients with type 1 diabetes who began intensive insulin therapy immediately after their initial diagnosis. The study utilized 81 patients with type 1 diabetes who fell into this treatment category. The authors determined that insulin resistance indicators, including waist circumference, waist-to-hip ratio, and triglyceride levels, were greater in cohort members with microangiopathy than in those without it. In addition, the estimated glucose disposal rate was lower in the microangiopathy patients than in the others. The authors concluded that an independent relationship exists between insulin resistance and the risk of microangiopathy in patients with diabetes type 1 who began receiving intensive insulin therapy right after their diagnosis.3
Pathophysiology
In insulin resistance, various clinical entities of this state are evident. The clinical heterogeneity can be explained, at least in part, on a biochemical basis. Insulin binds and acts mainly through the insulin receptor and also acts via the insulinlike growth factor–1 (IGF-1) receptor; cellular actions of insulin involve a wide variety of effects on postreceptor signaling pathways within target cells. The b subunit of the insulin receptor is a tyrosine kinase, which is activated when insulin binds to the a subunit; the kinase activity autophosphorylates and mediates multiple actions of insulin. Ambient insulin levels, various physiological and disease states, and drugs regulate insulin receptor concentration or affinity.
The mechanisms responsible for insulin resistance syndromes include genetic or primary target cell defects, autoantibodies to insulin, and accelerated insulin degradation.4 Obesity, the most common cause of insulin resistance, is associated with a decreased number of receptors and with postreceptor failure to activate tyrosine kinase. While adiposity and insulin resistance are related, they are not necessarily synonymous, and each may make independent and different contributions to increasing the risk of cardiovascular disease.1 Insulin resistance plays a major pathogenic role in the development of the metabolic syndrome, which may include any or all of the following:
•Hyperinsulinemia
•Type 2 diabetes or glucose intolerance
•Central obesity5 •Hypertension
•Dyslipidemia that includes high triglyceride levels
•Low HDL-C level and small, dense low-density lipoprotein (LDL) particles
•Hypercoagulability characterized by an increased plasminogen activator inhibitor–1 (PAI-1) level
Inflammation and adipocytokines probably play some role in the etiopathogenesis of metabolic syndrome.6,7 Increased levels of the acute-phase inflammatory marker C-reactive protein (CRP) are related to insulin resistance and the metabolic syndrome, suggesting a role for chronic, low-grade inflammation.8 In a number of prospective studies, increased levels of CRP predict the development of diabetes and cardiovascular disease.1 Reduced serum levels of adiponectin (a hormone made by fat tissue) and elevated leptin concentration are also features of conditions associated with the metabolic syndrome or cardiovascular disease.9,10,11,12
Omentin, a novel adipokine, is a protein expressed and secreted from visceral but not subcutaneous adipose tissue that increases insulin sensitivity in adipocytes. Plasma levels of omentin-1, the major circulating isoform, are inversely correlated with BMI, waist circumference, leptin levels, and insulin resistance syndrome and are positively correlated with adiponectin and HDL levels.13,14,15
Insulin sensitivity and secretion are reciprocally related; consequently, insulin resistance results in increased insulin secretion to maintain normal glucose and lipid homeostasis. The mathematical relationship between insulin sensitivity and secretion is curvilinear or hyperbolic. Several potential mediators are thought to signal the pancreatic B cells to respond to insulin resistance; these potential mediators include glucose, free fatty acids, autonomic nerves, fat-derived hormones (eg, adiponectin), and the gut hormone glucagonlike peptide 1 (GLP-1). GLP-1 is an incretin hormone that stimulates insulin secretion, causes B-cell mitosis while inhibiting apoptosis, inhibits glucagon secretion, and delays gastric emptying with overall antidiabetic effects.
Failure of the signals or of the pancreatic B cells to adapt adequately in relation to insulin sensitivity results in inappropriate insulin levels, IFG, IGT, and type 2 diabetes.
Glucose and lipid metabolism largely depend on mitochondria to generate energy in cells. Mitochondrial dysfunction may play an important role in the development of insulin resistance and associated complications.16
Insulin resistance, the compensatory hyperinsulinemia, and other components are associated with increased risk of cardiovascular disease; endothelial dysfunction is a prominent feature of insulin resistance syndrome. Type 2 diabetes is characterized by increased hepatic glucose output, increased peripheral resistance to insulin action (due to receptor and postreceptor defects), and impaired insulin secretion. In skeletal muscle, various abnormalities, including defective glucose transport, may cause insulin resistance. Glucose transporter 4 (GLUT-4) is the main insulin-responsive transporter. Insulin and IGFs are important regulators of ovarian function. Insulin resistance and hyperinsulinemia are thought to be responsible for the hyperandrogenism that is characteristic of the polycystic ovary syndrome. Other distinct manifestations of insulin resistance syndrome or related conditions involve various organs, as well as the skin.
Two major variants of insulin receptor abnormalities associated with acanthosis nigricans have been described—the classic type A insulin resistance syndrome, which is due to an absent or dysfunctional receptor, and type B insulin resistance syndrome, which results from autoantibodies to the insulin receptor. Both syndromes are associated with hyperinsulinemia. Hypoglycemia may still occur in some individuals with insulin resistance syndrome because of an agonist effect of autoantibodies on the insulin receptor. In some patients with insulin-binding antibodies, hypoglycemia may occur when insulin dissociates from the antibodies several hours after a meal.
Frequency
United States
The frequency of insulin resistance is observed to be 3% in the general population; a several-fold increase occurs in individuals with glucose intolerance.
International
Early studies indicated a more significant association between insulin resistance and the various components of the metabolic syndrome in white persons than in members of other ethnic groups. However, findings have since suggested a similar relationship in many minority populations. However, available systematic data apply mainly to white populations. Marked variations exist in methodologies and diagnostic criteria. Prevalence rates of insulin resistance syndrome reported for white populations ranged from 3-16%; a rate of less than 2% was reported among Japanese populations. A quarter of the world's adults are considered to have the metabolic syndrome.17
Mortality/Morbidity
Insulin resistance is a common basis for development of glucose intolerance, including diabetes and coronary artery disease.
•People with the metabolic syndrome are twice as likely to die from, and 3 times as likely to have, a myocardial infarction or stroke than are with people without the syndrome.
•People with the metabolic syndrome have a 5-fold increased risk of developing type 2 diabetes.
•Diabetes mellitus is the sixth leading cause of death by disease and the seventh leading cause of death in the United States. Globally, up to 80% of the 200 million people with diabetes will die of cardiovascular disease. Diabetes is the leading cause of end-stage renal disease and blindness in the United States. Individuals with diabetes have a much higher risk of heart disease and a higher risk of stroke; they also have a high risk of neuropathy and gangrene. Diabetes is also associated with acute metabolic complications.
•Coronary artery disease is the leading cause of death in the United States and in most developed countries. Coronary artery disease is responsible for 500,000 deaths annually in the United States. Nearly 1.5 million myocardial infarctions, approximately one third of which are fatal, occur annually. The total annual economic cost of coronary artery disease in the United States is nearly $60 billion.
•Mortality and morbidity related to other conditions associated with insulin resistance include the following:
◦Polycystic ovary syndrome - Infertility, menstrual irregularity, androgen excess
◦Rare conditions -Lipodystrophic states (fatty liver [Liver cirrhosis is a major cause of morbidity and mortality.])
◦Leprechaunism - Growth retardation, abnormal glucose homeostasis (especially occurrence of hypoglycemia), early death
Race
Insulin resistance syndrome is found in all races. The degree of clustering of the risk variables of the metabolic syndrome is generally considered to be higher among whites. However, prevalence rates of the various components of the metabolic syndrome tend to be higher among nonwhite populations.18
Acanthosis nigricans, a common physical sign of insulin resistance syndrome, occurs in all ethnic groups, but the prevalence is higher in Hispanics and blacks than it is in whites.
Sex
The metabolic syndrome is more evident in middle-aged men. Women tend to assume increased cardiovascular risk after menopause. PCOS is a disease limited to women. Type A and type B syndrome are typically found in women.
Age
The strongest relationship between insulin resistance and cardiovascular risk factors is observed in middle-aged persons rather than in older individuals, although cardiovascular morbidity and mortality increase with age.
•Women with PCOS usually present in their mid-20s.
•Many rare disorders of insulin resistance present in early life (eg, leprechaunism [first year of life], lipodystrophic states [ages 6-9 y until early puberty]).
•Type A insulin resistance typically occurs in younger patients, while type B insulin resistance occurs more often in older women.
Clinical
History
The presentation of insulin resistance depends on the type and stage of the insulin-resistant state. Most patients have 1 or more clinical features of the insulin-resistant state. Many patients do not develop overt diabetes despite extreme insulin resistance. Other patients present with cases of severe hyperglycemia that require large quantities of insulin (>200 units); these people may manifest the classic symptoms of diabetes mellitus, such as polyuria, polydipsia, polyphagia, and weight loss.
Patients may present with the following:
•Hypoglycemia - Some patients present with symptoms of hypoglycemia, such as sweating, tremulousness, irritability, and an altered level of consciousness. Hypoglycemia results from interaction between insulinomimetic antibodies and the insulin receptor. Some patients have insulin-binding antibodies directed against insulin, which, upon dissociation, can cause hypoglycemia.)
•Metabolic syndrome (syndrome X)
•Obesity (most common cause of insulin resistance) or history or excessive body weight
•Type 2 diabetes mellitus (chronic or acute [during severe decompensation] presentation [ie, the classic symptoms of diabetes])
•A diagnosis of IGT or of IFG levels
•History of biochemical abnormalities, such as dyslipidemia, detected during routine screening or workup for a cardiovascular disease
•History of hypertension
•Symptoms of coronary artery disease
•Symptoms related to other macrovascular disease (eg, stroke, peripheral vascular disease)
•Microvascular angina
•Polycystic ovary syndrome (PCOS) - Patients usually present with infertility associated with anovulation; menstrual irregularity, typically chronic; and symptoms related to androgen excess, such as frontal baldness and deepening of the voice.)
•Type B syndrome - Symptoms related to immunologic disease (eg, arthralgia, swollen salivary glands, hair loss) may occur.
•Other insulin-resistant states
◦Leprechaunism - Abnormal facial appearance, early life growth retardation
◦Lipodystrophic states - Insulin resistance, usually during childhood, with progression to diabetes over several years
◦Werner syndrome - Features of premature aging
◦Rabson-Mendenhall syndrome - Dental and nail abnormalities, skin lesions
◦Pineal hypertrophic syndrome - Dental and nail abnormalities, sexual precocity
◦Alstrom syndrome - Childhood blindness, impaired hearing
◦Ataxia-telangiectasia - Movement disorder and symptoms related to immune deficiency, such as increased proneness to pulmonary infections
◦Myotonic dystrophy - Muscle weakness and visual symptoms (cataract)
•Immune insulin resistance
◦Low titer immunoglobulin (Ig) G anti-insulin antibodies are present in most patients receiving insulin.
◦Patients with a history of interrupted exposure to beef insulin treatment are particularly prone to this resistance.
◦Clinically significant resistance usually occurs in patients with preexisting, significant tissue insensitivity to insulin (eg, obesity).
Physical
•Blood pressure (hypertension)
•Anthropometry
◦Waist or waist-to-hip ratio, height, weight, and BMI may indicate insulin resistance syndrome. This notion was supported by an Argentinian study of 625 children, 91 of whom were overweight and another 96 of whom were classified as obese.19 The investigators examined the association between insulin resistance and the following indexes: waist circumference, BMI, waist circumference/height, weight/(sitting height)(2), and waist circumference/sitting height. The study's results suggested that waist circumference and BMI are the anthropometric indexes that best correlate with the presence of insulin resistance.
◦Central obesity, not peripherally distributed fat, is a strong marker of insulin resistance syndrome.
•Cardiovascular system
◦Signs of heart disease
◦Peripheral vascular disease - Abnormalities in pulses and arterial wall
◦Stigmata of lipid disorders - Suggests the possibility of underlying hyperlipidemia
◦Premature arcus cornealis - Deposits of cholesterol and phospholipid
◦Xanthelasma - Indicates that lipid status should be investigated
◦Lipemia retinalis - Retinal vessels with milky, chylomicron-rich plasma commonly observed in acute, uncontrolled diabetes
◦Skin xanthomata - Eruptive xanthomas found most commonly on the buttocks
◦Tendon xanthomata - Usually over the patellar and Achilles tendon
•Type A syndrome
◦Patients are usually tall and have features of hirsutism and abnormalities of the female reproductive tract related to hyperandrogenism (eg, PCOS).
◦The patient may have either a thin or a muscular body build.
◦Acral enlargement, a form of pseudoacromegaly, is not uncommon.
•Acanthosis nigricans
◦Acanthosis nigricans is common in patients with type A syndrome; it causes patchy, velvety brown hyperpigmentation plaques that are usually found in flexural areas, especially in the axillae and the nuchal region.
◦Lesions may be due to the effect of high circulating levels of insulin on IGF receptors in the skin.
◦Acanthosis nigricans is found in a wide variety of clinical conditions that are associated with insulin resistance.
◦These eruptions have been reported in nearly one tenth of women evaluated for PCOS.
◦Acanthosis nigricans is occasionally a marker of malignant neoplasm.
•PCOS - Patients may have masculine habitus, such as coarse or greasy skin and acne, frontal alopecia, breast atrophy, hypertrophy of the clitoris, and obesity; varying degrees of hirsutism or virilization may be present. These manifestations are due to hyperandrogenism.
•Type B insulin resistance (autoantibodies to the insulin receptor) - Patients usually have symptomatic diabetes mellitus, although ketoacidosis is unusual. Patients occasionally present with hypoglycemia. Agonist activity (hypoglycemia) or antagonist effect (insulin resistance) can occur, depending on the site of binding to the insulin receptor.
•Other insulin-resistant states
◦Leprechaunism - Elfin appearance of the face, hirsutism, lack of subcutaneous fat, and thickened skin
◦Lipodystrophic states - Variable phenotypic expression (Features include a total or partial lack of adipose tissue, metabolic dysfunction, such as abnormal glucose homeostasis, hypertriglyceridemia, and increased metabolic rate.)
◦Werner syndrome - Cataract, atrophic skin, and early osteopenia
◦Rabson-Mendenhall syndrome - Dystrophic nails, dental dysplasia, and acanthosis nigricans
◦Pineal hypertrophic syndrome - Early dentition with malformed teeth, hirsutism, thick nails, and skin dryness
◦Alstrom syndrome - nerve deafness, hypogonadism (males), and retinal degeneration that results in blindness
◦Ataxia telangiectasia - Cerebellar ataxia, oculocutaneous telangiectases, immune deficiency, and increased proneness to pulmonary infections
◦Myotonic dystrophy - Weakness of limb and cranial muscles, cataract
Causes
Insulin resistance results from inherited and acquired influences. Hereditary causes include mutations of insulin receptor, glucose transporter, and signaling proteins, although the common forms are largely unidentified. Acquired causes include physical inactivity, diet, medications, hyperglycemia (glucose toxicity), increased free fatty acids, and the aging process.20
The underlying causes of insulin-resistant states can be categorized as follows:
•Prereceptor
◦Abnormal insulin (mutations)
◦Anti-insulin antibodies
•Receptor
◦Decreased number of receptors (mainly, failure to activate tyrosine kinase)
◦Reduced binding of insulin
◦Insulin receptor mutations
◦Insulin receptor – blocking antibodies
•Postreceptor
◦Defective signal transduction
◦Mutations of GLUT4 (In theory, these mutations could cause insulin resistance, but polymorphisms in the GLUT4 gene are rare.)
•Combinations of defects - Such combinations are common. Obesity is associated mainly with postreceptor abnormality and is also associated with a decreased number of insulin receptors. Obesity is the most common cause of insulin resistance.
•Other conditions that are categorized as receptor or postreceptor insulin-resistant states
◦Type A syndrome
◦Type B syndrome
◦Leprechaunism
◦Lipodystrophic states
◦Ataxia-telangiectasia
◦Werner syndrome
◦Rabson-Mendenhall syndrome
◦Pineal hypertrophic syndrome
•Aging - This may cause insulin resistance through a decreased production of GLUT-4
•Increased production of insulin antagonists - A number of disorders are associated with increased production of insulin antagonists, such as Cushing syndrome, acromegaly, and stress states, such as trauma, surgery, diabetes ketoacidosis, severe infection, uremia, and liver cirrhosis.
•Medications associated with insulin resistance syndrome - These include glucocorticoids (Cushing syndrome), cyclosporine, niacin, and protease inhibitors.
•Human immunodeficiency virus (HIV)21 - Protease inhibitor – associated lipodystrophy is a recognized entity.22 Nucleoside analogues have also been implicated in the development of insulin resistance.
•Insulin treatment
◦Low titer IgG anti-insulin antibody levels are present in most patients who receive insulin. In rare instances, the antibodies result in significant prereceptor insulin resistance.
◦Enhanced destruction of insulin at the site of subcutaneous injection has also been implicated.
More on Insulin Resistance
Overview: Insulin Resistance
Differential Diagnoses & Workup: Insulin Resistance
Treatment & Medication: Insulin Resistance
Follow-up: Insulin Resistance
References
Further Reading
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[ CLOSE WINDOW ]Further Reading
Related eMedicine topics:
Diabetes Mellitus, Type 2 [Endocrinology]
Diabetes Mellitus, Type 2 [Pediatrics: General Medicine]
Diabetes Mellitus, Type 2 - A Review
Glucose Intolerance
Lipodystrophy, Generalized
Obesity [Endocrinology]
Obesity [Pediatrics: General Medicine]
Polycystic Ovarian Syndrome [Obstetrics and Gynecology]
Polycystic Ovarian Syndrome [Pediatrics: General Medicine]
Polycystic Ovarian Disease (Stein-Leventhal Syndrome)
Clinical guidelines:
Prevention and treatment of pediatric obesity: an Endocrine Society clinical practice guideline. The Endocrine Society - Disease Specific Society. 2008 Dec. 38 pages. NGC:006944
Primary prevention of cardiovascular disease and type 2 diabetes in patients at metabolic risk: an Endocrine Society clinical practice guideline. The Endocrine Society - Disease Specific Society. 2008 Oct. 34 pages. NGC:006945
Clinical trials:
Alpha Lipoic Acid and Insulin Resistance
Chronic Hepatitis C and Insulin Resistance
Effect of Continuous Subcutaneous GHRP-3 Infusion at 2 Doses on the GH-IGF-I System, BP, Glucose, and Insulin Resistance
Mechanisms of Insulin Resistance in Humans
[ CLOSE WINDOW ]Keywordsinsulin resistance, diabetes insulin, metabolic syndrome, insulin resistant, fasting glucose, glucose tolerance, glucose tolerance test, type 2 diabetes mellitus
[ CLOSE WINDOW ]Contributor Information and DisclosuresAuthorSamuel T Olatunbosun, MD, FACP, Chief, Internal Medicine, 56th Medical Group, Luke Air Force Base
Samuel T Olatunbosun, MD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians-American Society of Internal Medicine, and American Diabetes Association
Disclosure: Nothing to disclose.
Coauthor(s)Samuel Dagogo-Jack, MD, MBBS, MSc, FRCP, Professor of Medicine, Program Director, Division of Endocrinology, Diabetes and Metabolism, University of Tennessee Health Science Center
Samuel Dagogo-Jack, MD, MBBS, MSc, FRCP is a member of the following medical societies: American College of Physicians, American Diabetes Association, American Federation for Medical Research, Endocrine Society, and Royal College of Physicians
Disclosure: Eli Lilly None Speaking and teaching; GlaxoSmithKline None Speaking and teaching; Merck None Speaking and teaching
Medical EditorDavid S Schade, MD, Chief, Division of Endocrinology and Metabolism, Professor, Department of Internal Medicine, University of New Mexico School of Medicine and Health Sciences Center
David S Schade, MD is a member of the following medical societies: American College of Physicians, American Diabetes Association, American Federation for Medical Research, Endocrine Society, New Mexico Medical Society, New York Academy of Sciences, and Society for Experimental Biology and Medicine
Disclosure: Nothing to disclose.
Pharmacy EditorFrancisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Managing EditorDon S Schalch, MD, Professor Emeritus, Department of Internal Medicine, Division of Endocrinology, University of Wisconsin Hospitals and Clinics
Don S Schalch, MD is a member of the following medical societies: American Diabetes Association, American Federation for Medical Research, Central Society for Clinical Research, and Endocrine Society
Disclosure: Nothing to disclose.
CME EditorMark Cooper, MBBS, PhD, FRACP, Head, Diabetes & Metabolism Division, Baker Heart Research Institute, Professor of Medicine, Monash University
Disclosure: Nothing to disclose.
Chief EditorGeorge T Griffing, MD, Professor of Medicine, St Louis University School of Medicine
George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.
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