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The metabolic syndrome: Insulin resistance

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Abstract

Insulin resistance is the most accepted unifying theory explaining the pathophysiology of the metabolic syndrome. However, epidemiologic studies indicate that a substantial proportion of patients with the metabolic syndrome do not have evidence of insulin resistance, and the correlation between insulin resistance and individual components of the syndrome is weak to moderate. Insulin resistance may play an important role in the development of hyperglycemia and dyslipidemia, which can further aggravate insulin resistance. The implication of insulin resistance in hypertension appears to be less strong than its role in causing hyperglycemia and dyslipidemia. Obesity may be another pathogenic factor in the metabolic syndrome that may help initiate or worsen insulin resistance. However, like insulin resistance, obesity is not universal in the metabolic syndrome, and many obese subjects do not have metabolic abnormalities. This review provides an update on the relationship between insulin resistance and main components of the metabolic syndrome: hyperglycemia, dyslipidemia, hypertension, and obesity.

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References and Recommended Reading

  1. Kahn R, Buse J, Ferrannini E, Stern M: The metabolic syndrome: time for a critical appraisal. Joint statement from the American Diabetes Association and the European Association for the study of diabetes. Diabetes Care 2005, 28:2289–2304.

    Article  PubMed  Google Scholar 

  2. Hanley AJG, Wagenknecht LE, D’Agostino RB, et al.: Identification of subjects with insulin resistance and b-cell dysfunction using alternative definitions of the metabolic syndrome 2003, 52:2740–2747.

    CAS  Google Scholar 

  3. Jeppesen J, Hansen TW, Rasmussen S, et al.: Insulin resistance, the metabolic syndrome, and risk of incident cardiovascular disease. J Am Coll Cardiol 2007, 49:2112–2119.

    Article  PubMed  CAS  Google Scholar 

  4. Yki-Jarvinen H: Glucose toxicity. Endocr Rev 1992, 13:415–431.

    PubMed  CAS  Google Scholar 

  5. Del Prato S, Leonetti F, Simonson DC, et al.: Effect of sustained physiologic hyperinsulinemia and hyperglycemia on insulin secretion and insulin sensitivity in man. Diabetologia 1994, 37:1025–1035.

    Article  PubMed  CAS  Google Scholar 

  6. Bertaccca A, Ciccarone A, Cecchetti P, et al.: Continually high insulin levels impair Akt phosphorylation and glucose transport in human myoblasts. Metabolism 2005, 54:1687–1693.

    Article  CAS  Google Scholar 

  7. Eckel RH, Grundy SM, Zimmet PZ: The metabolic syndrome. Lancet 2005, 365:1415–1428.

    Article  PubMed  CAS  Google Scholar 

  8. Ferrannini E, Barrett EJ, Bevilacqua S, De Fronzo RA: Effect of fatty acids on glucose production and utilization in man. J Clin Invest 1983, 72:1737–1747.

    Article  PubMed  CAS  Google Scholar 

  9. Anderson EA, Hoffman RP, Balon TW, et al.: Hyperinsulinemia produces both sympathetic neural activation and vasodilation in normal humans. J Clin Invest 1991, 87:2246–2252.

    Article  PubMed  CAS  Google Scholar 

  10. Strazzullo P, Barbato A, Galletti F, et al.: Abnormalities in renal sodium handling in the metabolic syndrome. Results of the Oliveti Heart Study. J Hyperten 2006, 24:1633–1639.

    Article  CAS  Google Scholar 

  11. Barbato A, Cappucio FP, Folkerd EJ, et al.: Metabolic syndrome and renal sodium handling in three ethnic groups living in England. Diabetologia 2004, 47:40–46.

    Article  PubMed  CAS  Google Scholar 

  12. Tuck ML, Bounoua F, Eslami P, et al.: Insulin stimulates endogenous angiotensin II production via a mitogen-activated protein kinase pathway in vascular smooth muscle cells. J Hypertens 2004, 22:1779–1785.

    Article  PubMed  CAS  Google Scholar 

  13. Fallo F, Veglio F, Bertello C, et al.: Prevalence and characteristics of the metabolic syndrome in primary hyperaldosteronism. J Clin Endocrinol Metab 2006, 91:454–459.

    Article  PubMed  CAS  Google Scholar 

  14. Mikhail N, Tuck M: Insulin and the vasculature. Curr Hypertens Rep 2000, 2:148–153.

    Article  PubMed  CAS  Google Scholar 

  15. Laasko M, Edelman S, Brechtel G, Baron A: Decreased effect of insulin to stimulate skeletal muscle blood flow in obese man. A novel mechanism for insulin resistance. J Clin Invest 1990, 85:1844–1852.

    Article  Google Scholar 

  16. Laasko M, Edelman S, Brechtel G, Baron A: Impaired insulin-mediated skeletal muscle blood flow in patients with NIDDM. Diabetes 1992, 41:1076–1083.

    Article  Google Scholar 

  17. Natali A, Taddei S, Galvan AQ, et al.: Insulin sensitivity, vascular reactivity and clamp-induced vasodilatation in essential hypertension. Circulation 1996, 96:849–855.

    Google Scholar 

  18. Mikhail N, Golub M, Tuck M: Obesity and hypertension. Prog Cardiovasc Dis 1999, 42:39–58.

    Article  PubMed  CAS  Google Scholar 

  19. Carr DB, Utzschneider KM, Hull RL, et al.: Intra-abdominal fat is a major determinant of the National Cholesterol Education Program Adult Treatment Panel III Criteria for the metabolic syndrome. Diabetes 2004, 53:2087–2094.

    Article  PubMed  CAS  Google Scholar 

  20. Wildman RP, Munter P, Reynolds K, et al.: The obese without cardiometabolic risk factor clustering and the normal weight with cardiometabolic risk factor clustering. Prevalence and correlates of 2 phenotypes among the US population (NHANES 1999–2004). Arch Intern Med 2008, 168:1617–1624.

    Article  PubMed  Google Scholar 

  21. Klein S, Fontana L, Young L, et al.: Absence of an effect of liposuction on insulin action and risk factors for coronary heart disease. N Engl J Med 2004, 350:2549–2557.

    Article  PubMed  CAS  Google Scholar 

  22. Thorne A, Lonngvist F, Apelman J, et al.: A pilot study of long-term effects of a novel obesity treatment: omentectomy in connection with adjustable gastric banding. Int J Obes Relat Metab Disord 2002, 26:193–199.

    Article  PubMed  CAS  Google Scholar 

  23. Csendes A, Maluenda F, Burgos AM: A prospective randomized study comparing patients with morbid obesity submitted to laporotomic gastric bypass with or without omentectomy. Obes Surg 2008 (Epub ahead of print).

  24. Stefan N, Kantartzis K, Machann J, et al.: Identification and characterization of metabolically benign obesity in humans. Arch Intern Med 2008, 168:1609–1616.

    Article  PubMed  Google Scholar 

  25. Petersen KF, Dufour S, Befroy D, et al.: Impaired mitochondrial activity in the insulin-resistant offspring of patients with type 2 diabetes. N Engl J Med 2004, 350:664–671.

    Article  PubMed  CAS  Google Scholar 

  26. De Feyter HM, van den Broek NMA, Praet SFE, et al.: Early or advanced stage type 2 diabetes is not accompanied by in vivo skeletal muscle mitochondrial dysfunction. Eur J Endocrinol 2008, 158:643–653.

    Article  PubMed  CAS  Google Scholar 

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  1. MSc Division of Endocrinology, Department of Medicine, Olive-UCLA Medical Center, 14445 Olive View Drive, Sylmar, CA, 91342, USA

    Nasser Mikhail

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  1. Nasser Mikhail
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Correspondence to Nasser Mikhail.

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Mikhail, N. The metabolic syndrome: Insulin resistance. Current Science Inc 11, 156–158 (2009). https://doi.org/10.1007/s11906-009-0027-4

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