The Association Between C - reactive protein and Metabolic Syndrome Components

Öz

Background: Insulin resistance is associated with metabolic syndrome and is a risk factor for cardiovascular disease. C-reactive protein (CRP) is an inflammatory marker which is demonstrated as a strong predictor of future cardiovascular events. Material Method: In this study, sixty-three patients who were diagnosed with metabolic syndrome and twenty healthy controls were recruited. Fasting blood glucose, insulin and CRP levels were measured. Homeostasis Model Assessment (HOMA-IR) formula is used to evaluate insulin resistance. We investigated the relationship between insulin resistance and CRP levels and whether CRP is a metabolic syndrome criterion or not. Results: There were statistically significant differences between patients with metabolic syndrome and controls in terms of waist circumference, fasting glucose, insulin and CRP levels. In patients, we found a poor but significant relationship between fasting glucose levels and CRP (P=0.0001, r=0.3) and between HOMA-IR values and CRP (P=0.007, r=0.29). Conclusion: We concluded that CRP may have an important role in the diagnosis and follow-up of metabolic syndrome. Key words: Diabetes, Metabolic syndrome, CRP, HOMA, Insulin resistance, Waist circumference

Anahtar Kelimeler

• Diabetes, Metabolic syndrome, CRP, HOMA, Insulin resistance, Waist circumference

CRP ile Metabolik Sendrom Arasındaki İlişki

Öz

Giriş: İnsülin direnci metabolik sendrom ile ilişkilidir ve kardiyovasküler hastalıklar için risk faktörüdür. C-Reaktif protein (CRP) gelecekteki kardiyovasküler hastalıkların habercisi olan bir proinflamatuar belirteçdir. Biz bu çalışmada insülin direnci ile CRP düzeylerinin ilişkisini ve CRP'nin metabolik sendromda kriter olup olmayacağını araştırdık. Gereç ve Yöntem: Bu çalışmaya metabolik sendrom tanısı almış 63 hasta ile 20 sağlıklı kontrol grubu dahil edildi. Açlık kan glukoz seviyeleri, insülin ve CRP düzeyleri ölçüldü. İnsülin dirençleri (Homeostasis Model Assessment=HOMA-IR) formülü kullanılarak değerlendirildi. Bulgular: Metabolik sendromlu hasta grubu ile kontrol grubu arasında bel çevresi, açlık glukozu, insülin ve CRP değerleri arasında istatistiksel anlamlı farklılıklar vardı.Hasta grubunda açlık glukoz düzeyleri ve CRP arasında (P=0,0001, r=0,3) ve HOMA-IR ile CRP arasında (P=0,007, r=0,29) zayıf fakat anlamlı bir ilişki vardı. Sonuç: CRP'nin metabolik sendromun tanı ve takibinde önemli bir parametre olduğu sonucuna vardık. Anahtar kelimeler: Diabet, Metabolik sendrom, CRP, HOMA, İnsülin direnci, Bel çevresi

Anahtar Kelimeler

• Diabet, Metabolik sendrom, CRP, HOMA, İnsülin direnci, Bel çevresi

Kaynakça

1. Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). JAMA 2001; 285(19):2486-97.
2. Sansoy V, Ersanlı M. Koroner Kalp Hastaligi Koruma ve Tedavi Kilavuzu. Turk Kardioloji Dernegi Ars 2002; 30:568-94.
3. Unwin N, Shaw J, Zimmet P, et al. Alberti KG. Impaired glucose tolerance and impaire fasting glycemia: The current status on definition and intervention . Diabet Med 2002;19(9):708-23.
4. Khaw K, Warehan N, Luben R, et al. Glycated hemoglobin, diabetes and mortality in men in Norfolk cohort of European prospective investigation of cancer and nutrition. BMJ 2001; 322:15-8.
5. Gotto A, Pownall H. Manual of Lipid Disorders. Baltimore, Williams and Wilkins, 1999; 18-44.
6. Will new diagnostic criteria for diabetes mellitus change phenotype of patients with diabetes? Reanalysis of European Diabetes Epidemiology study Group. BMJ 1998; 317:371-5.
7. Isıldak M, Guven SG, Gurlek A. Metabolik sendrom ve insulin direnci. Hacettepe Tip Dergisi 2004; 35:96.
8. Rich SS, Bowden DW, Haffner SM et al. Identification of quantitative trait loci for glucose homeostasis. The Insulin Resistance Atherosclerosis Study (IRAS) Family Study. Diabetes 2004; 53:1866-75.

9. De-Frozo RA, Tobin JD, Anders R. Glucose clamp technique: a method for quantifying insulin secretion and resistance. Am. J Physiol 1979; 237:14-223.
10. American Diabetes Association . Consensus development conference on insulin resistance. Diabetes Care 1998; 21(2):310-4.
11. Matthews DR, Hosker JP, Rudenski AS, et al. Homeostasis model assesment: Insuline resistance and ß-cell function from fasting plasma glucose and insuline concentrations in man. Diabetologia 1985; 28:412-9.
12. Matsumoto K, Miyake S, Yaro M, et al. Glucose tolerance, insulin secretion, and insulin sensitivity in nonobese and obese Japanese subjects. Diabetes Care 1997; 20:1562-8.
13. Haffner SM, Gonzales C, Miettiner H, et al. A prospective analysis of the HOMA model: the Mexico City Diabetes Study. Diabetes Care 1996; 19:1138-41.
14. Nagasako S, Imamato Y, Ishikama S, et al. Efficocy of troglitazone measured by insulin resistance index (letter). Lancet 1997;350:184.
15. Ersanlı E. Insulin direnci ve sonucları. Turk Kardioloji Dernegi Lipid Gundemi 2003; 32:1-12.
16. Ford ES, Ajani UA, Mokdad AH. The metabolic syndrome and concentrations of C-reactive protein among U.S. youth. Diabetes Care 2005; 28(4):878-8l.
17. Reaven GM. Role of insulin resistance in human disease. Diabetes 1988;37:1895- 907.
18. Ridker PM, Rifai N, Rose L, et al. Comparison of C-Reactive Protein and low density lipoprotein cholesterol levels in the predicton of first cardiovascular events. N Engl J Med 2002; 347(20):1557-65.
19. Fröhlich M, Imhof A. Association between C-Reactive protein and features of the metabolic syndrome. Diabetes Care 2000; 23:1835-9.
20. Jialal I, Deveraj S, Venugopal SK. C-Reactive Protein: Risk marker or mediator in atherothrombosis? Hypertension 2004; 44:6-11.
21. Sjoholm A, Nyström T.Inflammation and the etiology of type 2 diabetes. Diabetes Metab Res Rev 2006; 22:4-10.
22. Corresponding Author: Dr.Alev KURAL
23. Ataköy 9. kısım A2Blok B Giriş No:92
24. Bakırköy Istanbul/TURKEY
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