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© Borgis - Postępy Nauk Medycznych 9/2011, s. 745-748
*Marta Włodarczyk, Agnieszka Jarosz, Grażyna Nowicka
Inflammatory markers in men with metabolic syndrome genotyped to -455G/A polymorphism in beta-fibrinogen gene
Markery stanu zapalnego a polimorfizm -455G/A genu dla fibrynogenu u mężczyzn z zespołem metabolicznym
Department of Nutrigenomics of the National Food and Nutrition Institute in Warsaw, Poland
Head: prof. Grażyna Nowicka
Streszczenie
Rozwój procesu zapalnego niskiego rzędu jest cechą charakterystyczną pacjentów z zespołem metabolicznym i w istotny sposób determinuje ryzyko wystąpienia incydentów klinicznych w obrębie układu sercowo-naczyniowego. Poziom rozwoju procesu zapalnego zależy od wielu czynników metabolicznych i genetycznych. W prezentowanej pracy oceniano związek między polimorfizmem -455G/A genu dla fibrynogenu a poziomem CRP i molekuł adhezyjnych. Badaniem objęto 61 mężczyzn z rozpoznanym zespołem metabolicznym. Poziom cząsteczek adhezyjnych (VCAM-1 i ICAM-1) określano metodą immunoenzymatyczną (ELISA). Stężenie CRP oznaczono metodą immunoturbidymetryczną. Polimorfizm -455G/A genu dla fibrynogenu wykrywano metodą PCR z wykorzystaniem enzymu restrykcyjnego. W badanej grupie mężczyzn z zespołem metabolicznym częstość genotypu GG wynosiła 60%, genotypu GA – 33%, zaś genotypu AA – 7%. Zaobserwowano wyższe stężenia fibrynogenu, CRP i molekuł adhezyjnych u nosicieli allela A w porównaniu z homozygotami GG. Różnice te były niezależne od wartości BMI oraz stężenia lipidów i glukozy.
Summary
Low-grade inflammation is a characteristic feature of metabolic syndrome and significantly contributes to cardiovascular risk in affected subjects. The level of inflammatory process development is influenced by different metabolic and genetic factors. In the present study the association between -455G/A genetic variants in fibrinogen gene and plasma levels of CRP and adhesion molecules was assessed in 61 men with newly diagnosed metabolic syndrome. DNA was amplified by polymerase chain reaction and incubated with the restriction enzyme. Circulating levels of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were measured by enzyme-linked immunosorbent assay (ELISA). Serum high-sensitivity CRP was determined by immunoturbidimetric method. The -455G/A genotype frequencies were 60%, 22%, and 7% for GG, GA, and AA, respectively. It was found that fibrinogen, CRP and adhesion molecules concentrations were enhanced in A-allele carriers as compared to GG homozygotes, and these differences were not related to BMI, and serum lipids and glucose levels.
INTRODUCTION
Metabolic syndrome (MS) as a constellation of risk factors of cardiovascular disease, has received increased attention in the last years, because growing prevalence of MS has been notice in epidemiological and clinical observations (1, 2). MS development is strongly related to improper diet and low physical activity, therefore obesity is one of the important features of MS. However, there is no doubts that different metabolic and genetic factors may influence both metabolic syndrome development and the level of associated cardiovascular risk (3, 4). A role for inflammation in cardiovascular diseases development has become well established over the past decade (5). It has been also accepted that low grade inflammatory process is a key feature of metabolic syndrome strongly influencing associated cardiovascular risk (6, 7). There is no doubts that the intensity of inflammation dependents on many factors (7, 8). Plasma concentrations of fibrinogen have been found to be associated with cardiovascular risk (9). However, it is uncertain whether this association is causal or reflects residual confounding of other risk factors. Genetic variants that influence lifelong differences in plasma fibrinogen levels have not been found to be strongly associated with CVD risk, but there is a lack of data describing potential effect of such variants on inflammatory process development. Therefore, the aim of the presented study was to assess the relationship between occurrence of -455G/A genetic variants in beta-fibrinogen gene and serum levels of C-reactive protein and adhesion molecules in patients with metabolic syndrome.
EXPERIMENTAL PROCEDURES
Patients with metabolic syndrome were recruited for the study among these referred to the Outpatient Clinic of Metabolic Diseases of National Food and Nutrition Institute, who underwent a complete physical examination. Metabolic syndrome was defined according to the Third Report of the National Cholesterol Education Program’s Adult Treatment Panel. MS was recognized when any three or more of following criteria were found: waist circumference > 102 cm in men and > 88 cm in women, serum triglycerides ≥ 150 mg/dl, blood pressure ≥ 130/85 mmHg, HDL-cholesterol < 40 mg/dl in men and < 50 mg/dl in women, serum glucose ≥ 110 mg/dl
Venous blood was collected from each individual after fasting. Plasma total and high-density lipoprotein, triglycerides and glucose were measured by routine methods. CRP concentrations were determined by ultra sensitive assay from Randox. Enzyme immunoassays were used to determine serum levels of ICAM-1 and VCAM-1 (Endogen). Fibrinogen levels were assayed by immunoturbidimetric method based on reagents from DAKO. The plasma levels of adiponectin and leptin were measured by ELISA using reagent kits from Linco Research and Bio Vendor, respectively. DNA was extracted from whole blood with a DNA Blood Mini Kit (A&A biotechnology). The -455G/A polymorphism in the promoter region of the beta-fibrinogen gene was genotyped by PCR amplification of genomic DNA, followed by restriction enzyme digestion (HaeIII) and agarose gel electrophoresis according to procedure described by Thomas et al (10). Data were analyzed using InStat computer package (GraphPad Software,USA).
RESULTS

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Piśmiennictwo
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15. Zdrojewski T, Babińska Z, Bondosz K, Wyrzykowski B: Epidemiology of obesity and visceral obesity in Poland West Europe and USA (Epidemiologia otyłości i otyłości brzusznej w Polsce, Europie Zachodniej i USA). Kard Prakt 2004; 3: 3-7.
16. Ridker PM, Pare G, Parker A et al.: Loci related to metabolic-syndrome pathways including LEPR, HNF1A, IL6R and GCKR associate with plasma C-reactive protein: Women’s Genome Health Study. Am J Hum Genet 2008; 82: 1185-92.
otrzymano: 2011-07-12
zaakceptowano do druku: 2011-08-10

Adres do korespondencji:
*Marta Włodarczyk
Department of Nutrigenomics National Food and Nutrition Institute
str. Powsinska 61/63, 02-903 Warszawa
tel.: (22) 550-97-48
e-mail: mwlodarczyk@izz.waw.pl

Postępy Nauk Medycznych 9/2011
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