Association of plasminogen activator inhibitor-1 and tissue plasminogen activator with type 2 diabetes and metabolic syndrome in Malaysian subjects

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Association of plasminogen activator inhibitor-1 and tissue plasminogen activator with type 2 diabetes and metabolic syndrome in Malaysian subjects
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  ORIGINAL INVESTIGATION Open Access Association of plasminogen activator inhibitor-1and tissue plasminogen activator with type 2diabetes and metabolic syndrome inMalaysian subjects Zaid Al-Hamodi 1* , Ikram S Ismail 2 , Riyadh Saif-Ali 1,3 , Khaled A Ahmed 4 , Sekaran Muniandy 1* Abstract Background: Increased plasma plasminogen activator inhibitor-1 (PAI-1) activity and decreased tissue plasminogenactivator (tPA) activity could be considered a true component of the metabolic syndrome (MetS) associated withan increased risk of developing cardiovascular diseases (CVD) and fibrinolytic abnormalities. The aim of this studywas to investigate the association of tPA and its inhibitor PAI-1 with type 2 diabetes (T2D) and MetS andinterrelationship between PAI-1and tPA activities and antigens in Malaysian T2D and normal subjects. Methods: The plasma activities and antigens of PAI-1 and tPA and the levels of the tPA/PAI-1 complex as well asserum insulin, parameter of the coronary risk panel and plasma glucose at fasting state were studied in 303 T2Dsubjects (227 with MetS and 76 without MetS), 131 normal non-diabetic non-metabolic subjects and 101 non-diabetic MetS subjects. Results: The PAI-1 activity was higher in subjects with T2D with MetS (P = 9.8 × 10 -19 ) and non-diabetic subjectswith MetS (P = 3.0 × 10 -15 ), whereas the tPA activity was lower in T2D with MetS (P = 0.003) as compare to normalsubjects. Plasma tPA antigen levels were higher in subjects with T2D with MetS (P = 8.9 × 10 -24 ), T2D without MetS(P = 1.3 × 10 -13 ) and non-diabetic MetS subjects (P = 0.002). The activity and antigen of PAI-1 in normal subjectswere related to insulin resistance (P = 2.2 × 10 -4 ; 0.007). Additionally, the PAI-1 activity was associated with anincreased waist circumference (P = 2.2 × 10 -4 ) and decreased HDL-c (P = 0.005), whereas the tPA activity wasassociated with decreased FBG (P = 0.028). The highest correlation was between PAI-1 activity and its antigen(R 2 = 0.695, P = 1.1 × 10 -36 ) in diabetic subjects. The tPA activity negatively correlated with its antigen (R 2 = -0.444,P = 7.7 × 10 -13 ) in normal subjects and with the PAI-1 activity and antigen (R 2 = -0.319, P = 9.9 × 10 -12 ; R2 = -0.228,P = 3.4 × 10 -6 ) in diabetic subjects. Conclusions: PAI-1 and tPA activities and antigens were associated with diabetes and MetS parameters inMalaysian subjects. Background Central obesity, hyperglycaemia, high triglycerides (TG),low high-density lipoprotein cholesterol (HDL-c) andhypertension, all are well-documented risk factors fortype 2 diabetes (T2D) and cardiovascular diseases(CVD)[1]. The constellation of these metabolic abnormalities(known as a metabolic syndrome (MetS) or insulin resis-tance syndrome) increases the risk of T2D and CVD.The number of individuals with the MetS has increasedglobally during the past two decades, and this increaseis associated with the worldwide epidemic of obesity and diabetes [2]. Obesity and physical inactivity are thedriving forces for MetS and a person with MetS has 5-fold higher relative risk to develop diabetes [3] and 2.5fold higher to develop CVD [4,5]. Overweightedness and * Correspondence:zalhamodi@yahoo.com;sekaran@um.edu.my 1 Department of Molecular Medicine, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, MalaysiaFull list of author information is available at the end of the article Al-Hamodi et al  . Cardiovascular Diabetology  2011, 10 :23http://www.cardiab.com/content/10/1/23 C ARDIO V ASCULAR  D IABETOLOGY © 2011 Al-Hamodi et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the CreativeCommons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, andreproduction in any medium, provided the srcinal work is properly cited.  obesity lead to adverse effects on blood pressure, choles-terol, TG and impaired glucose tolerance (IGT) [6].Plasminogen activator inhibitor-1 (PAI-1) is the pri-mary physiological inhibitor of endogenous fibrinolysisthat acts via inhibition of the tissue plasminogen activa-tor (tPA) and the urokinase type activator (uPA), oftenleading to fibrin accumulation in basement membranesand interstitial tissues [7-9]. Elevations in plasma PAI-1 appear to compromise normal fibrin clearance mechan-isms and promote thrombosis. The plasminogen activa-tors (t-PA and u-PA) convert plasminogen to plasmin,which is involved in fibrinolysis, tissue remodelling andcell migration [10]. In addition to its role in intravascu-lar fibrinolysis, PAI-1 is also involved in cell-associatedproteolysis, cell migration, and tissue remodelling play-ing a role in pathological processes such as cancer cellinvasion, metastasis and inflammation [11,12]. The majority of tPA in the blood is bound to its primary inhibitor, PAI-1[13].In large epidemiological studies elevated plasma PAI-1has been demonstrated in various subgroups as animportant feature of T2D and MetS [14-20] and this elevation may contribute to a thrombotic tendency [7-9,15,21]. This elevation precedes coronary artery dis- ease [22] and even predicts the occurrence of first acutemyocardial infarction and reinfarction [23-25]. Remark- ably, the predictive ability of PAI-1 disappears afteradjustment for markers of the MetS [26,27], suggesting that the MetS is a prerequisite to high plasma PAI-1levels in patients prone to atherothrombosis. Moreover,it has been hypothesized that PAI-1 participates in thedevelopment of key features of the MetS. The circulat-ing PAI-1 levels are positively associated with obesity and insulin resistance [28-30]. tPA activity may be an independent and early markerfor asymptomatic lower extremity arterial disease inT2D [18,31]. Plasma tPA activities and the capacity of  endothelial cells to secret tPA in response to a fibrino-lytic stimulus were also reported to be decreased inadults with diabetes [15]. Elevated plasma tPA antigenshave been reported to be associated with insulin resis-tance, T2D, and obesity [14,18] and increased risk of  CHD [32].The aim of this study was to investigate the associa-tion of the plasma activities and antigens of PAI-1 andtPA, with T2D and MetS and to study the relationshipbetween activities and antigens of PAI-1 and tPA. Materials and methods Subjects and data collection This study involved diabetic patients with and withoutMetS and non-diabetic subjects with MetS receivingtreatment at the University Malaya Medical Centre(UMMC), Kuala Lumpur. Normal subjects withoutdiabetes and MetS (the control group) in Klang Valley,Kuala Lumpur were recruited. The study was approvedby the Medical Ethics Committee of University MalayaMedical Centre. Written informed consent was obtainedfrom each subject. Patients with acute or chronic infec-tions, severe medical conditions (malignancy, renalfailure, liver cirrhosis, connective tissue disease, andchronic congestive heart failure) and pregnant womenwere excluded from the study.Blood pressure (BP) measurements were taken fromeach patient ’ s right arm in the seated position by usingan Omron IntelliSense Automatic Blood Pressure Moni-tor after 10 min of rest in a quiet room in the morning.Two to three successive BP readings were obtained at5-min intervals and averaged. Body weight and heightwere measured in the fasting state without shoes in themorning, and BMI was computed as weight in kilograms(kg) divided by height in meters squared (m 2 ). Waist cir-cumference was measured midway between the lowerrib margin and the superior iliac spine at the end of gentle expiration in a standing position.Fasting venous blood (10ml) was collected from eachsubject within a 2-hour window (8:00 to 10:00 AM)after 15 minutes rest, because of the diurnal variation of plasma PAI-1 [33]. The collected blood immediately taken into four labelled Vacutainer tubes, 0.109Mtrisodium citrate (for tPA and PAI-1 antigens and tPA/PAI-1 complex analysis), acidified 0.5M sodium citrate(for tPA and PAI-1 activities), sodium fluoride (for glu-cose measurement) and plain tubes (for insulin and lipidprofile). The plasma/serum of trisodium citrate andplain tubes were separated gently within 30 minutes by using Allerga R X-12R centrifuge (Beckman Coulter. IncUS) for a 15 min at 2500-3000 × g at 4°C. Then theplasma/serum was separated into corresponding microtubes and immediately kept at -80°C until analysis. Biochemical Analyses Serum TG, HDL-c and plasma glucose (FPG) were mea-sured by an automated analyzer Dimension ® RxL Max ® Integrated Chemistry System. Insulin was measured by ADVIA Centaur assay XP Immunoassay System(Siemens Healthcare Diagnostics Inc. Deerfield, ILUSA). All these investigations were done at ClinicalDiagnostic Laboratory of the University Malaya MedicalCentre (UMMC), Kuala Lumpur. Insulin resistance (IR)and Insulin sensitivity (IS) were calculated using theHomeostasis Model Assessment (HOMA2) Calculator v2.2 which is available from Oxford Centre for Diabetes,Endocrinology and Metabolism.Plasma PAI-1 antigen was measured by TintElize ® PAI-1 antigen ELISA test from Biopool (Trinity BiotechInc. USA, Jamestown, NY). PAI-1 activity, tPA activity and antigen and tPA/PAI-1complex were measured by  Al-Hamodi et al  . Cardiovascular Diabetology  2011, 10 :23http://www.cardiab.com/content/10/1/23Page 2 of 9  PAI-1 activity, tPA activity, tPA total antigen, tPA/PAI-1complex human assays respectively, (Molecular Innova-tions, Inc. Peary Court, Novi, MI USA) according to themanufacturer ’ s instructions. Plates were read at 450nmexcept the PAI-1 antigen plate which was at 490nmusing a microplate reader (BioRad, USA). Statistical Analyses The results were analyzed by the SPSS 11.5 (SocialPackage of Statistical Science) computer program by LEAD Technologies; Inc. USA). The missing data werelistwise deleted (when any of the variables were missing,the entire observation was omitted from the analysis).The age, body mass index (BMI), waist, systolic bloodpressure (SBP), diastolic blood pressure (DBP), TG,HDL-c, FBS, insulin, IS, IR, PAI-1 and tPA activities andantigens and tPA/PAI-1 complex were log transformedbecause they were not normally distributed. Theseparameters means and 95% confidence intervals weretransformed back and reported as geometric means. Theassociation of PAI-1 and tPA activities and antigens andtPA/PAI-1 complex with T2D and MetS were assessedby univariate analyses (general linear model) adjustedfor age, gender and race as covariates. The associationof fibrinolytic PAI-1 and tPA activities and antigenswith MetS parameters; (BMI, waist, SBP, DBP, TG,HDL-c, FBS, insulin, IS and HOMA (IR) (dependent variables) were analysed by hierarchical linear regressionadjusted for age, gender and race as covariates in nor-mal subjects. The interrelationship between fibrinolyticparameters; PAI-1 and tPA activities and antigens andtPA/PAI-1 complex in normal and T2D subjects werefirst evaluated by linear regression. This evaluationshowed that (BMI, HDL-c and IR), (HDL-c and IR),(FBS), (Age and IS) and (BMI) were significantly asso-ciated with PAI-1 activity, PAI-1 antigen, tPA activity,tPA antigen and tPA/PAI-1 complex respectively. Thenthe correlation of fibrinolytic parameters with eachother re-evaluated by hierarchical linear regression con-trolled for those corresponding confounder in additionto age, gender and race. Results Of five hundred normal subjects freely respondents, only 190 were recruited for the study. After biochemical testsand application of IDF criteria for MetS diagnosis [34],131 subjects were revealed as normal without diabetesand MetS (the control group). One hundred and onesubjects out of 142 participants under treatment forhyperlipidaemia and/or hypertension at University Malaya Medical Centre (UMMC) were diagnosed asnon-diabetic MetS subjects. Three hundred and threesubjects who were previously diagnosed as T2D wereparticipated in this study. Of these, 227 had MetS and76 did not have MetS as defined by the IDF criteria forMetS diagnosis.The demography and biochemical parameters of thesubjects are shown in table1. The fibrinolytic para-meters, PAI-1 and tPA activities and antigens and tPA/PAI-1 complex assessed by general linear model (uni- variate) are shown in table2. In general, the plasmalevels of PAI-1 activity and tPA antigens were higher inT2D patients compared to normal subjects (P = 1.7 ×10 -8 , 3.0 × 10 -24 respectively) whereas the PAI-1 antigenand tPA activity (P = 0.01, 0.03 respectively) were lowerin T2D. There was no difference in tPA/PAI-1 complexbetween T2D and control subjects. On the other hand,the plasma PAI-1 activity was higher in non-diabeticMetS (P = 3.0 × 10 -15 , 1.5 × 10 -18 ) and T2D with MetSsubjects (P = 9.8 × 10 -19 , 1.8 × 10 -21 ) compared to nor-mal and T2D without MetS subjects respectively. Never-theless, there was no difference in PAI-1 activity between the normal and T2D without MetS subjectsand between non-diabetic MetS and T2D with MetSsubjects (Table2). However, the PAI-1 antigen was notsignificantly higher in non-diabetic MetS and signifi-cantly lower in T2D without MetS (P = 2.2 × 10 -9 ) com-pared to normal subjects. The results further showedthat PAI-1 antigen was lower in both T2D withoutMetS (P = 6.9 × 10 -13 ) and T2D with MetS (P = 0.02)compared to non-diabetic MetS subjects. Besides, it washigher in T2D with MetS (P = 5.1 × 10 -10 ) compared toT2D without MetS subjects. The tPA activity was lowerin T2D with MetS compared to normal, non-diabeticMetS and T2D without MetS groups (P = 0.003, 0.002,6.7 × 10 -5 ) respectively. On the other hand, there wereno differences in the tPA activities between the othergroups. In contrast, the tPA antigen was higher in non-diabetic MetS, T2D without MetS and T2D with MetScompared to control group (P = 0.002, 1.3 × 10 -13 , 8.9 ×10 -24 ) respectively. In addition, the tPA antigen washigher in T2D without MetS and T2D with MetScompared to non-diabetic MetS group (P = 1.3 × 10 -6 ,1.3 × 10 -12 ) respectively. Further the results showed thattPA/PAI-1 complex was lower in the T2D withoutMetS compared to normal (P = 0.04), non-diabeticMetS (P = 0.02) and T2D with MetS (p = 0.001) groupswhile there were no differences in the tPA/PAI-1 com-plex between the other groups.The association of fibrinolytic variables (PAI-1 andtPA activities and antigens) with MetS parameters wasevaluated in normal subjects, and the results aredepicted in table3. The activity and antigen of PAI-1associated with increased insulin levels (b = 1.941,P = 1.2 × 10 -4 ; b = 1.614, P = 0.015), insulin resistance(b = 1.393, P = 2.2 × 10 -4 ; b = 1.318, P = 0.007), anddecreased insulin sensitivity (b = -1.963, P = 1.1 × 10 -4 ;b = -1.637, P = 0.012). Furthermore, the PAI-1 activity  Al-Hamodi et al  . Cardiovascular Diabetology  2011, 10 :23http://www.cardiab.com/content/10/1/23Page 3 of 9  associated with an increased waist circumference (b =1.159, P = 2.2 × 10 -4 ) and BMI (b = 1.199, P = 0.001))and decreased HDL-c levels (b = -1.125, P = 0.005.).Although the tPA activity counteracts the PAI-1 activity which associated with decreased FBG (b = -1.079, P =0.028), the tPA antigen showed no association withMetS parameters.The interrelationship between activities and antigensof PAI-1 and tPA and tPA/PAI-1 complex parameterswere further assessed in normal and T2D groups asshown in Table4and5respectively. Among normal subjects, the tPA activity negatively correlated with itsantigen (r 2 = -0.44, P = 7.7 × 10 -13 ) and weakly corre-lated with tPA/PAI-1 complex (r 2 = -0.090, P = 0.001).In contrast, the tPA antigen positively correlated withtPA/PAI-1 complex (r 2 = 0.202, P = 3.5 × 10 -7 ). Unlikenormal subjects, there was a good correlation betweenfibrinolytic parameters in T2D, the PAI-1 activity welland positively correlated with its antigen (r 2 = 0.70, P =1.1 × 10 -36 ), and negatively correlated with tPA activity (r 2 = -0.32, P = 9.9 × 10 -12 ). A similar correlation wasshown between PAI-1 antigen and tPA activity (r 2 =-0.23, P = 3.4 × 10 -6 ). The pattern of tPA antigen corre-lation with tPA/PAI-1 complex among T2D was similarto that in normal subjects, but it was a weak correlation(r 2 = -0.20, P = 3.5 × 10 -7 ; r 2 = 0.06, P = 7.9 × 10 -5 ). Discussion The Association of fibrinolytic parameters with T2D andmetabolic syndrome were studied; a higher PAI-1 activ-ity is associated with T2D with MetS and MetS (nondia-betic), which is characterized by the presence of  Table 1 Demography and Biochemical parameters among normal, non-diabetic metabolic syndrome and type 2diabetes with and without metabolic syndrome groups Parameters Normal (n = 131) Non-diabetic MetS(n = 101)Type 2 diabeteswithout MetS (n = 76) with MetS (n = 227)Gender% Male/ Female 18.5/29.2 23.9/14.8 17.7/11.3 39.9/44.7 Malay 25.9 17.5 13.7 43.0 Races % Chinese 36.1 22.1 14.8 27.0 Indian 12.1 18.8 14.8 54.4 Age (yrs) 47.2(44.9-49.7) 52.1(50.0-54.3) 49.8(47.6-52.1) 51.4(50.5-52.4) p-value a 0.003 a 0.349 a 0.002 Body Mass Index (kg/m2) 22.7(22.1-23.3) 27.2(26.4-28.0) 23.34(22.5-24.3) 29.8(29.2-30.3) p-value a 3.8 × 10 -13 a 0.515, b 6.2 × 10 -10 a 3.8 × 10 -13  , b 3.2 × 10 -6  , c  3.8 × 10 -13 Waist circumference (cm) 79.2(77.4-81.1) 94.5(92.8-96.3) 82.9(80.7-85.2) 98.6(97.4-99.7) p-value a 3.8 × 10 -13 a 0.02 , b 4.2 × 10 -13 a 3.8 × 10 -13  , b 0.006, c  3.8× 10 -13 Diastolic Blood Pressure(mmHg) 80.0(78.4-81.5) 85.6(83.6-87.6) 79.3(77.1-81.5) 83.1(81.7-84.5) p-value a 1.7 × 10 -4 a 0.966, b  2.3 × 10 -4 a 0.02 , b 0.004 , c 0.02 Systolic Blood Pressure (mmHg) 130(127-134) 139(136-143) 129(125-134) 136(134-139) p-value a 0.002 a 0.965 , b 0.002 a 0.02 , c 0.02 Triglyceride (mmol/l) 1.08(1.00-1.17) 1.59(1.46-1.72) 1.38(1.19-1.57) 1.78(1.66-1.91) p-value a 1.6 × 10 -6 a 0.02 a 3.6 × 10 -13  , c  0.001 High Density Lipoprotein(mmol/l) 1.54(1.48-1.61) 1.26(1.20-1.31) 1.22(1.15-1.29) 1.15(1.11-1.18) p-value a 1.2 × 10 -10 a  2.6 × 10 -12 a 4.8 × 10 -13  , b 0.008 Fasting Blood Glucose (mmol/l) 5.02(4.93-5.10) 5.36(5.23-5.49) 8.05(7.41-8.74) 7.74(7.39-8.11) p-value 0.24 a a 3.8 × 10 -13  , b 3.8 × 10 -13 a 3.8 × 10 -13  , b 3.8 × 10 -13 Insulin (pmol/l) 45.7(41.7-50.1) 77.3(69.6-85.8) 63.7(52.9-76.5) 120(110-131) p-value a 7.3 × 10 -9  a 0.002 a 4.1 × 10 -13  , b 5.0 × 10 -8  , c  1.4 × 10 -12 Insulin resistance (IR) 0.91(0.83-1.01) 1.53(1.37-1.69) 1.49(1.24-1.77) 2.59(2.38-2.81) p-value a 1.0 × 10 -6 a 3.2 × 10 -5 a 4.1 × 10 -13  , b  2.5 × 10 -12  , c  3.8 × 10 11  The result presented as geometric mean and 95% confidence interval of mean, a vs control group: b vs non-diabetic metabolic syndrome group: c vs type 2diabetes without metabolic syndrome which evaluated by ANOVA. Bolt values are significant. MetS: metabolic syndrome. Al-Hamodi et al  . Cardiovascular Diabetology  2011, 10 :23http://www.cardiab.com/content/10/1/23Page 4 of 9  abdominal obesity and insulin resistance; this result inagreement with other studies [35-40]. The plasma PAI-1 circulates in two states, active and latent. Active PAI-1is bound to vitronectin (VN) [41,42] (the net molecular weight of PAI-1/vitronectin, ~125,000) while latent PAI-1 is unbound (MW ~50,000). The plasma vitronectinlevels are increased in diabetes with nephropathy [43].T2D subjects with renal failure were excluded from thisstudy. However, nephropathy in T2D starts from theearly stage of development diabetes. Thus the latentPAI-1 may be excreted in urine in quantities more thanPAI-1/vitronectin complex, which may result in anincrease in the ratio of active to latent PAI-1 in T2Dcompared to normal subjects. This may explain why PAI-1 antigen is lower in T2D while PAI-1 activity ishigher.The Association of fibrinolytic parameters with MetSparameters was assessed in normal (control subjects),since the diabetic and non-diabetic MetS under treat-ment. There was a clear trend shows increasing of PAI-1 activity with increased insulin resistance, waist circum-ference, BMI, and decreased HDL-c. This would alsoexplain the non-association of PAI-1 activity in subjectswith T2D but without MetS.PA1-1 is partly synthesised in fat cells, and its activity is related to abdominal obesity as mirrored by the highwaist circumference [44]. In this regard, lipid infusion innormal subjects to the levels observed in T2D, and Table 2 Comparison of fibrinolytic PAI-1 and tPA between normal, non-diabetic metabolic syndrome, type 2 diabeteswith and without metabolic syndrome and total type 2 diabetes groups Parameters Normal (n = 131) Non-diabetic MetS(n = 101)Type 2 diabetes Total Type 2diabetes (n = 303)without MetS(n = 76)with MetS (n = 227)PAI-1 activity (IU/ml) 12.8(11.1-14.7) 28.7(25.1-32.8) 11.0(9.37-12.9) 29.0(26.1-32.1) 21.7(19.7-23.9) p-value a 3.0 × 10 -15  , c  1.5 ×10 -18 a 0.167 a 9.8 × 10 -19   , c  1.8 × 10 -21 a 1.7 × 10 -8  , b 0.02 PAI-1 antigen (ng/ml) 30.2(27.1-33.7) 33.0(29.7-36.6) 18.2(16.2-20.6) 28.4(26.5-30.5) 25.4(23.9-27.1) p-value a 0.259 a  2.2 × 10 -9   , b 6.9 × 10 -13 b 0.02 , c 5.1 × 10 -10 a 0.01 , b 4.7 × 10 -5 tPA activity (U/ml) 3.49(3.11-3.92) 3.51(3.14-3.91) 3.91(3.42-4.47) 2.82(2.58-3.07) 3.11(2.89-3.34) p-value a 0.965 a 0. 206 a 0.003 , b 0.002 , c 6.7 × 10 -5 a 0.03 , b 0.03 tPA antigen (ng/ml) 4.62(4.10-5.21) 5.99(5.35-6.70) 9.15(8.04-10.4) 9.85(9.14-10.6) 9.67(9.07-10.31) p-value a 0.002 a 1.3 × 10 -13  , b 1.3 × 10 -6 a 8.9 × 10 -24  , b 1.3 × 10 -12 a 3.0 × 10 -24  , b 1.7 × 10 -12 tPA/PAI-1 complex (ng/ml) 3.50(2.89-4.23) 3.57(2.97-4.30) 2.59(2.09-3.20) 3.91(3.46-4.42) 3.52(3.17-3.92) p-value a 0.879 a 0.04 , b 0.02 a 0.336, c 0.001 a 0.94  The result presented as geometric mean and 95% confidence interval of mean adjusted for age, gender and race, a vs control group: b vs non-diabetic metabolicsyndrome group: c vs type 2 diabetes without metabolic syndrome which evaluated by univariate (General Linear Model). Bolt values are significant. MetS:metabolic syndrome. Table 3 Association of fibrinolytic PAI-1 and tPA with metabolic syndrome parameters among normal subjects(n = 131) Metabolic syndrome Parameters PAI-1 activityb (P-value)PAI-1 antigenb (P-value)tPA activityb (P-value)tPA antigenb (P-value)Body Mass Index (kg/m2) 1.199 (0.001) 1.079 (0.199) -1.109 (0.104) -1.021 (0.783) Waist circumference (cm) 1.159 (2.2 × 10 -4  ) 1.057 (0.213) -1.033 (0.496) -1.035 (0.543) Diastolic Blood Pressure (mmHg) -1.038 (0.342) -1.014 (0.763) 1.064 (0.185) 1.028 (0.607) Systolic Blood Pressure (mmHg) -1.009 (0.846) 1.007 (0.889) 1.074 (0.198) 1.084 (0.195) Triglyceride (mmol/l) 1.119 (0.165) -1.012 (0.899) 1.064 (0.558) 1.127 (0.331) HDL- cholesterol (mmol/l) -1.125 (0.005) -1.067 (0.166) -1.076 (0.174) -1.016 (0.807) Fasting Blood Sugar (mmol/l) 1.047 (0.092) 1.079 (0.02) -1.079 (0.028) 1.023 (0.583) Insulin (pmol/l) 1.941 (1.2 × 10 -4  ) 1.614 (0.015) -1.236- (0.312) 1.288 (0.298) Insulin Sensitivity (%) -1.963 (1.1 × 10 -4  ) -1.637 (0.012) 1.265 (0.266) -1.294 (0.289) Insulin Resistance 1.393 (2.2 × 10 -4  ) 1.318 (0.007) -1.119 (0.305) 1.135 (0.313) Result presented as b (P-value) assessed by linear regression, adjusted for age, gender and race. Bolt values are significant. b: coefficient for the relationshipbetween the dependent variable “ metabolic syndrome parameters ” and the independent variable “ fibrinolytic PAI-1 and tPA parameters ” . The positive sign of thecoefficient implies a direct relationship, and the negative sing implies an inverse relationship. Al-Hamodi et al  . Cardiovascular Diabetology  2011, 10 :23http://www.cardiab.com/content/10/1/23Page 5 of 9
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