Insulin Resistance Article – Archived

-::- Note: The below is published here for archival purposes -::-
Thanks to for this invaluable article

Insulin Resistance


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:

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


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:

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.


- - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -
An automatic insert of some related ads:

Thanks for your patronage. Article continues below:
- - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -

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.


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.


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.



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).


  • 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


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.


  1. Lee SH, Park SA, Ko SH, et al. Insulin resistance and inflammation may have an additional role in the link between cystatin C and cardiovascular disease in type 2 diabetes mellitus patients. Metabolism. Sep 16 2009;[Medline].
  2. American Association of Clinical Endocrinologists position statement on metabolic and cardiovascular consequences of polycystic ovary syndrome. Endocr Pract. Mar-Apr 2005;11(2):126-34. [Medline].
  3. Uruska A, Araszkiewicz A, Zozulinska-Ziolkiewicz D, et al. Insulin Resistance is Associated with Microangiopathy in Type 1 Diabetic Patients Treated with Intensive Insulin Therapy from the Onset of Disease. Exp Clin Endocrinol Diabetes. Apr 6 2010;[Medline].
  4. Reaven GM. Pathophysiology of insulin resistance in human disease. Physiol Rev. 1995;75(3):473-86. [Medline].
  5. Reaven G, Abbasi F, McLaughlin T. Obesity, insulin resistance, and cardiovascular disease. Recent Prog Horm Res. 2004;59:207-23. [Medline][Full Text].
  6. de Luca C, Olefsky JM. Inflammation and insulin resistance. FEBS Lett. Jan 9 2008;582(1):97-105. [Medline].
  7. Tilg H, Moschen AR. Inflammatory mechanisms in the regulation of insulin resistance. Mol Med. Mar-Apr 2008;14(3-4):222-31. [Medline][Full Text].
  8. Florez H, Castillo-Florez S, Mendez A. C-reactive protein is elevated in obese patients with the metabolic syndrome. Diabetes Res Clin Pract. Jul 4 2005;[Medline].
  9. Semple RK, Cochran EK, Soos MA, et al. Plasma adiponectin as a marker of insulin receptor dysfunction: clinical utility in severe insulin resistance. Diabetes Care. May 2008;31(5):977-9. [Medline].
  10. Brabant G, Müller G, Horn R, et al. Hepatic leptin signaling in obesity. FASEB J. Jun 2005;19(8):1048-50. [Medline][Full Text].
  11. Fuke Y, Fujita T, Satomura A, et al. Alterations of insulin resistance and the serum adiponectin level in patients with type 2 diabetes mellitus under the usual antihypertensive dosage of telmisartan treatment. Diabetes Technol Ther. May 2010;12(5):393-8. [Medline].
  12. Meilleur KG, Doumatey A, Huang H, et al. Circulating Adiponectin Is Associated with Obesity and Serum Lipids in West Africans. J Clin Endocrinol Metab. Apr 9 2010;[Medline].
  13. de Souza Batista CM, Yang RZ, Lee MJ, et al. Omentin plasma levels and gene expression are decreased in obesity. Diabetes. Jun 2007;56(6):1655-61. [Medline].
  14. Tan BK, Adya R, Farhatullah S, et al. Omentin-1, a novel adipokine, is decreased in overweight insulin-resistant women with polycystic ovary syndrome: ex vivo and in vivo regulation of omentin-1 by insulin and glucose. Diabetes. Apr 2008;57(4):801-8. [Medline][Full Text].
  15. Moreno-Navarrete JM, Catalan V, Ortega F, et al. Circulating omentin concentration increases after weight loss. Nutr Metab (Lond). Apr 9 2010;7(1):27. [Medline].
  16. Kim JA, Wei Y, Sowers JR. Role of mitochondrial dysfunction in insulin resistance. Circ Res. Feb 29 2008;102(4):401-14. [Medline].
  17. Moadab MH, Kelishadi R, Hashemipour M, et al. The prevalence of impaired fasting glucose and type 2 diabetes in a population-based sample of overweight/obese children in the Middle East. Pediatr Diabetes. Sep 18 2009;[Medline].
  18. Beck-Nielsen H. General characteristics of the insulin resistance syndrome: prevalence and heritability. European Group for the study of Insulin Resistance (EGIR). Drugs. 1999;58 Suppl 1:7-10; discussion 75-82. [Medline].
  19. Hirschler V, Ruiz A, Romero T, et al. Comparison of different anthropometric indices for identifying insulin resistance in schoolchildren. Diabetes Technol Ther. Sep 2009;11(9):615-21. [Medline].
  20. Lutsey PL, Steffen LM, Stevens J. Dietary intake and the development of the metabolic syndrome: the Atherosclerosis Risk in Communities study. Circulation. Feb 12 2008;117(6):754-61. [Medline].
  21. [Best Evidence] De Wit S, Sabin CA, Weber R, et al. Incidence and risk factors for new-onset diabetes in HIV-infected patients: the Data Collection on Adverse Events of Anti-HIV Drugs (D:A:D) study. Diabetes Care. Jun 2008;31(6):1224-9. [Medline].
  22. Wierzbicki AS, Purdon SD, Hardman TC, et al. HIV lipodystrophy and its metabolic consequences: implications for clinical practice. Curr Med Res Opin. Mar 2008;24(3):609-24. [Medline].
  23. Lee WJ, Lee YC, Ser KH, et al. Improvement of insulin resistance after obesity surgery: a comparison of gastric banding and bypass procedures. Obes Surg. Mar 4 2008;[Medline].
  24. Hawley JA, Lessard SJ. Exercise training-induced improvements in insulin action. Acta Physiol (Oxf). Jan 2008;192(1):127-35. [Medline].
  25. Shih KC, Janckila AJ, Kwok CF, et al. Effects of exercise on insulin sensitivity, inflammatory cytokines, and serum tartrate-resistant acid phosphatase 5a in obese Chinese male adolescents. Metabolism. Sep 16 2009;[Medline].
  26. Jensterle M, Janez A, Mlinar B, et al. Impact of metformin and rosiglitazone treatment on glucose transporter 4 mRNA expression in women with polycystic ovary syndrome. Eur J Endocrinol. Jun 2008;158(6):793-801. [Medline].
  27. Salpeter SR, Buckley NS, Kahn JA, et al. Meta-analysis: metformin treatment in persons at risk for diabetes mellitus. Am J Med. Feb 2008;121(2):149-157.e2. [Medline].
  28. Quinn CE, Hamilton PK, Lockhart CJ, et al. Thiazolidinediones: effects on insulin resistance and the cardiovascular system. Br J Pharmacol. Feb 2008;153(4):636-45. [Medline].
  29. Savino A, Pelliccia P, Chiarelli F, et al. Obesity-related renal injury in childhood. Horm Res Paediatr. 2010;73(5):303-11. [Medline].
  30. Ahrén B, Pacini G. Islet adaptation to insulin resistance: mechanisms and implications for intervention. Diabetes Obes Metab. Jan 2005;7(1):2-8. [Medline].

-::- Note: The above is published here for archival purposes -::-
Thanks to for this invaluable article

Please visit their website to read the full article and support their efforts!

Source URL: Retrieved on: 8/18/2010

An automatic insert of a related ad:

Thanks for your patronage.

If you enjoyed this article you may enjoy these as well

Tags: , , , , , , , , , , , , , , ,

One Response to “Insulin Resistance Article – Archived”

  1. Insulin resistance, Glucose, Glycemic Index and IGF-1 | World Hair Research Says:

    [...] Read more about Insulin Resistance here. [...]

Leave a Reply

four − 3 =

Disclaimer: I must say this: The information presented herein is for informational purposes only. Consult your doctor, practitioner, and/or pharmacist for any health problem and before using any supplements, making dietary changes, or before making any changes in prescribed medications.
All posts are strictly opinions meant to foster debate, education, comment, teaching, scholarship and research under the "fair use doctrine" in Section 107 of U.S. Code Title 17. No statement of fact is made and/or should be implied. Please verify all the articles on this site for yourself. The Information found here should in no way to be construed as medical advice. If You have a health issue please consult your professional medical provider. Everything here is the authors own personal opinion as reported by authors based on their personal perception and interpretation as a part of authors freedom of speech. Nothing reported here should be taken as medical advice, diagnosis or prescription; medical advice should only be taken from your health care provider. Consume the information found on this web site under your own responsibility. Please, do your own research; reach your own conclusions, and take personal responsibility and personal control of your health.