Ponad 7000 publikacji medycznych!
Statystyki za 2021 rok:
odsłony: 8 805 378
Artykuły w Czytelni Medycznej o SARS-CoV-2/Covid-19

Poniżej zamieściliśmy fragment artykułu. Informacja nt. dostępu do pełnej treści artykułu
© 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
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.
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.

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.
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).

Powyżej zamieściliśmy fragment artykułu, do którego możesz uzyskać pełny dostęp.
Mam kod dostępu
  • Aby uzyskać płatny dostęp do pełnej treści powyższego artykułu albo wszystkich artykułów (w zależności od wybranej opcji), należy wprowadzić kod.
  • Wprowadzając kod, akceptują Państwo treść Regulaminu oraz potwierdzają zapoznanie się z nim.
  • Aby kupić kod proszę skorzystać z jednej z poniższych opcji.

Opcja #1


  • dostęp do tego artykułu
  • dostęp na 7 dni

uzyskany kod musi być wprowadzony na stronie artykułu, do którego został wykupiony

Opcja #2


  • dostęp do tego i pozostałych ponad 7000 artykułów
  • dostęp na 30 dni
  • najpopularniejsza opcja

Opcja #3


  • dostęp do tego i pozostałych ponad 7000 artykułów
  • dostęp na 90 dni
  • oszczędzasz 28 zł
1. Haffner S, Taegtmeyer H: Epidemic of obesity and the metabolic syndrome. Circulation 2003; 108: 1541-8.
2. Ford ES: Prevalence of the metabolic syndrome defined by the International Diabetes Federation among US adults in the U.S. Diabetic Care 2005; 28: 2745-9.
3. Lakka HM, Laaksonen DE, Lakka TA et al.: The metabolic syndrome and the total and cardiovascular disease mortality in middle-aged men. JAMA 2002; 288: 2709-17.
4. Nowicka G, Walczak A, Naruszewicz M: The role of genetic factors in the development of metabolic disorders associated with cardiovascular risk. [In:] Metabolic tratment of coronary heart disease, ed. A. Beresiewicz, M. Dłużniewski. Via Medica, Gdańsk 2006; pp. 67-89.
5. Nowicka G: Pathogenesis of atherosclerosis – the role of inflammation. Pol J Hum Nutr Metab 2005; 22, 245-51.
6. Devaraj S, Rosenson RS, Jialal I: Metabolic syndrome: an appraisal of the proinflammatory and procoagulant status. Endocrinol Metab Clin North Am 2004; 33: 3120-27.
7. Devaraj S, Valleggi S, Siegel D, Jialal I: Role of C-reactive protein in contributing to increased cardiovascular risk in metabolic syndrome. Curr Atheroscle Rep 2010; 12: 110-18.
8. Aromson D, Bartha P, Zinder O et al.: Obesity is the major determinant of elevated C-reactive protein in subjects with the metabolic syndrome. Intern J Obes 2004; 28: 674- 82.
9. Tousoulis D, Papageorgiou N, Androulakis A, et al. Fibrinogen and cardiovascular disease: Genetics and biomarkers. Blood Rev 2011; doi:10.1016/j.blre.2011.05.001
10. Thomas A, Green F, Kelleher C, Wilkes P et al.: Variation in the promoter region of the beta-fibrinogen gene is associated with plasma fibrinogen levels in smokers and non-smokers. Thromb Haemostasis 1991; 65: 487-90.
11. National Programme for the Prevention of Overweight and Obesity and Non-communicable Diseases through Diet and Improved Physical Activity 2007-2016. Ed. M. Jarosz. national Food and Nutrition Institute, Warsaw 2006.
12. Suzuki T, Katz R, Jenny NS et al.: Metabolic syndrome, inflammation, and incident heart failure in the elderly: the Cardiovascular Health Study. Circ Heart Fail 2008; 1: 242-8.
13. Pischon T, Hu FB, Rexrode KM et al.: Inflammation, the metabolic syndrome and risk of coronary heart disease in women and men. Atherosclerosis 2008; 197: 392-9.
14. Zuliani G, Volpato S, Galvani M et al.: Elevated C-reactive protein levels and metabolic syndrome in the elderly: the role of central obesity, data from the InChianti study. Atherosclerosis 2009; 203: 626-32.
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
Strona internetowa czasopisma Postępy Nauk Medycznych