Pkistn Journl of Nutrition 15 (3): 238-243, 2016 ISSN 1680-5194 Asin Network for Scientific Informtion, 2016 Hyperuricemi nd its Assocition with the Presence of Metolic Syndrome mong Indonesin Oese Adolescents 1,2 1,2 1,2 1,2 1,2 Adriyn Prmono, Nurynto, Etis Adi Murwni, Binr Pnunggl nd Geml Anjni 1 2 Deprtment of Nutrition, Center of Nutrition Reserch (CENURE), Fculty of Medicine, Diponegoro University, Semrng, Centrl Jv, Indonesi Astrct: Metolic syndrome (MetS) plys n importnt role in inflmmtion nd insulin resistnce. Incresing numer of dolescents MetS were common mong oese. The inflmmtory iomrkers my contriute to incresing levels of uric cid (UA). Currently UA is not only ssocited with gout, ut lso crdiovsculr disese. This ws cross sectionl study conducted in Semrng City, Indonesi. Consecutive smpling for oese dolescents ws dministrted. Aout 81 oese dolescents from two government highs schools were recruited in this study. We mesured nthropometry (weight, height, wist circumference, neck circumference), clinicl dt (systolic nd distolic lood pressure) nd iochemicl dt (triglyceride, HDL-cholesterol, fsting lood glucose, uric cid). A sujects ws ctegorized s MetS if presence 3 or more components of MetS. Gender nd Hyperuricemi ws ssocited with presence of MetS (p = 0.048 nd p = 0.004). The men levels of UA incresed ccordnce to the mount of MetS components (p = 0.000). Regression logistic nlysis concluded tht hyperuricemi s mjor risk fctor of MetS mong oese dolescents (OR = 3.97). Hyperuricemi contriuted to metolic syndrome mong Indonesin oese dolescents. Key words: Hyperuricemi, metolic syndrome, oese dolescents INTRODUCTION Oesity nd metolic syndrome hve een incresed in developing countries (Lloyd et l., 2012). Indonesi Ntionl Primry Helth Survey 2013 indicted significntly incresed of oesity in Indonesi dolescents from 1.7% in 2007 to 7.3% in 2013. Centrl oesity mong Indonesin people ws lso elevted significntly from 18.8% in 2007 to 26.6% in 2013 (Indonesin Bsic Helth Report, 2013). The incidence of metolic syndrome (MetS) increses with the incresing incidence of oesity. The condition of metolic syndrome (MetS) is ssocited with some inflmmtory processes tht ws chrcterized y elevtion of proinflmtor gents e.g., C-Rective Protein (CRP), Tumor Necrosis Fctor-" (TNF-"), Interferon-gmm (IFN-(), Interleukin (IL)-6 nd recently ws IL-18 (Thmn nd Aror, 2013). Inflmmtory iomrkers re then ssocited with therosclerotic vsculr disese process s comoridities of metolic syndrome. Some of studies expected tht therosclerotic vsculr disese ssocited with uric cid (UA) levels, with uncler metolic disorder s meditor (Lippi et l., 2008). The norml UA levels function s neuroprotective gent is lredy estlished. However, some studies reveled tht high level of uric cid hve een ssocited with therosclerotic vsculr disese, insulin resistnce nd metolic syndrome (Nghm et l., 2004). Uric cid levels >5.5 mg/dl hs een ssocited with crdiovsculr risk (Feig et l., 2008). Hyperuricemi led to declining of endothelil nitric oxide. Decresing of endothelil nitric oxide induced vsculr prolifertion nd endothelil dysfunction (Knellis nd Kng, 2005). The ssocition etween UA nd therosclerotic vsculr disese is still eing controverted due to indirect ssocition nd the possiility of metolic syndrome s origintor of Hyperuricemi nd therosclerotic vsculr disese. There re five risk fctors for metolic syndrome dignosis: centrl oesity y mesuring wist circumference, elevted triglyceride levels, decresed levels of HDL (High Density Lipoprotein), incresed lood pressure nd insulin resistnce seen with n increse in fsting lood glucose levels (Grundy et l., 2004). Through five risk fctors for the metolic syndrome, the metolic syndrome dignosis mong children nd dolescents were divided into two groups: the pre-metolic syndrome (Pr-MetS) with 1 or 2 risk fctors nd metolic syndrome (MetS) group with >3 risk fctors (Zimmet et l., 2007). It is lredy known tht therosclerosis stges hve egn since children nd dolescents (McGill et l., 2000). Incresing prevlence of dolescent s metolic syndrome nd oesity my ttriute to tht condition. The ssocition of single fctors or more of metolic syndrome nd Hyperuricemi mong oese Corresponding Author: Adriyn Prmono, Deprtment of Nutrition, Fculty of Medicine, Diponegoro University. Jl. Dr. Sutomo No. 18 Semrng-50231, Indonesi 238
MATERIALS AND METHODS Sujects, criteri nd nthropometry mesurement: This ws cross-sectionl study performed etween July of 2015 nd Septemer of 2015, pproved y the Reserch Committee of Diponegoro University, Fculty of Medicine numer 594/EC/FK-RSDK/2015. A convenience smple ws used. Inclusion criteri in this study ws dolescents ged etween 15 nd 18 yers old. Sujects who hd ny chronic disese such s secondry hypertension, type 1 dietes mellitus, dignosis of inflmmtory process, consume lcohol, smokers, or who were using mediction tht interfered with glucose metolism or lipids, such s steroids nd nti-inflmmtion, were excluded. A totl of 81 sujects were recruited in this study. Severl nthropometry mesurement ws conducted in this study. Weight ws mesured using clirted digitl ody weight scle (ccurcy 0.1 kg). Height ws mesured using sttur meter (ccurcy 0.1 cm). Body Mss Index (BMI) ws clculted using Weight (kg) 2 divided with Height (m ). Considering the following ctegories: oesity (z score + 2 < BMI < z score + 3) nd severe oesity (BMI > z score + 3), the WHO (2007) reference ws pointed out (WHO, 2007). Wist circumference (WC) ws mesured using nonstretchle tpe in the midpoint etween the lowest ri nd the ilic crest (Klein et l., 2007). Neck circumference (NC) ws mesured using sec 203 in the middle of the neck, etween the middle of the cervicl spine nd neck nterior mid nd suject stnding upright (Aswthpp et l., 2013). Girls with WC>90 percentile were considered s hving ltered WC. This study cutoff 90 percentile levels of WC for girls ws 87 cm nd oys 93 cm. Cutoff vlues for NC were otined from this study (Ferretti et l., 2015) which were ctegorized girls with ltered NC>32.65 cm nd oys> 37.95 cm. Pk. J. Nutr., 15 (3): 238-243, 2016 dolescents hs never een investigted in developing nlyst gripped out 3 cc venous loods. The DiSys countries. In spite of mny studies documented the Ct No. 20144 regents ws eing used in the nlysis reltionship etween the presences of MetS with UA in of the fsting lood glucose. Triglyceride (TG) ws dults ut still few studies ws oserved in children nlyzed using enzymtic method (Beckmn TG nd dolescents in developing countries. This study Regent). Mgnesium-dextrn sulfte precipittion imed to exmine the ssocition etween the regent ws used to seprte HDL cholesterol (HDL-c) presence of metolic syndrome nd Hyperuricemi from lipid complex. Fsting lood glucose, uric cid, mong oese dolescents. HDL-c nd TG were quntified using enzymtic method (Roche Cos Mir S28-6537, Roche Dignostics, Swizterlnd). Biochemicl mesurement ws conducted in ccredited lortory. Hyperuricemi ws considered with vlues >5.5 mg/dl (Feig et l., 2008). The dignosis of MetS ws otined using the criteri recommended y the Ntionl Cholesterol Eduction Progrm/Adult Tretment Pnel (NCEP/ATP) III (NCEP, 2002) dpted to the dolescents, which considers the presence of MetS s t lest three of the following items: WC>90 percentile (girls>87 cm nd oys>93 cm); TG>110 nd HDL-c<40 mg/dl, fsting lood glucose >100 mg/dl, SBP nd DBP>125 nd 75 mmhg (Tng et l., 2010). Sttisticl nlysis: The dt were presented s proportions, mens nd stndrd devitions (SD). After pplying the Kolmogorov-Smirnoff test to ssess for normlity, the ssocition of uric cid levels with gender, nutritionl sttus, WC, NC, SBP, DBP, TG, fsting lood glucose, HDL-c nd MetS ws demonstrted using the chi-squred or Fisher s exct test, when necessry, with 95% confidence intervl (95% CI) nd prevlence rtio (PR). The differences levels of uric cid on the numer of risk fctors of metolic syndrome were performed using one-wy nlysis of Vrince (ANOVA) test. The results of ANOVA test ws continued with Bonferroni s post hoc test. Logistic-regression ws used for vrile djustment, whose criterion for vrile inclusion ws the ssocition with the dependent vrile in the ivrite nlysis with p vlue<0.20. The vriles were included in the regression nlysis using the enter method, ccording to the decresing vlue of odds rtio. The Hosmer-Lemeshow test ws used s mesure of qulity-of-fit for the logistic-regression models, in which p-vlue>0.05 indictes tht the model is djusted. All nlyses were performed using the Sttisticl Pckge for Socil Sciences (SPSS Inc, Chicgo, US). Mesurement of MetS iochemicl indictors nd uric RESULTS cid: All suject were informed to do t lest 10 h fsting A totl of 81 oese dolescents completed this study. All egn t 10 m t Indonesi time efore loods sujects were tken from two middle-up socil economy collection. Two lood pressure mesurements were sttus high school in Semrng City re. Proportion of scled with 2 min intervl using riester femles in this study ws 49.4% vs. mles suject sphygmomnometer nd ws operted y well-trined 50.6%, with men of ge 15.77±1.06. Of the 81 sujects, generl prctitioner. The men of two mesurements men of BMI ws 30.05±4.95. The prevlence of MetS ws considered s the systolic (SBP) nd distolic mong oese dolescents ws 42.0% (56.1% mong (DBP) lood pressure vlues. Well-trined lortory mles nd 27.5% mong femles). Men of UA levels in 239
Pk. J. Nutr., 15 (3): 238-243, 2016 ll sujects ws 6.84±2.05 (3.40-13.90), with men mong mles suject 7.48±2.30 nd femles suject 6.19±1.53 (Tle 1). Systolic Blood Pressure ws high in 34.6% (28 of 81) nd DBP in 54.3% (44 of 81) of the oese dolescents. High levels of Triglyceride were descried in 17.3% (14 of 81) mong the sujects. Low levels of HDL-C were oserved in 70.3% (57 of 81 sujects) mong oese dolescents. Hyperglycemi ws oserved in only 1.2% of the sujects (Tle 2). Tle 2 represents gender nd presence of metolic syndrome ssocited with Hyperuricemi. It shows tht the risk to hve Hyperuricemi ws higher in the resulting groups: Mles oese (PR = 2.64) nd oese dolescents with MetS (PR = 4.68). The men concentrtions of UA were significntly different etween the components of MetS (p = 0.006). They incresed with the numer of the components of MetS. There ws significntly differences etween 1 nd 2 components of MetS vs. 4 components of MetS (2.11 (95% CI, 0.06-4.16) with p = 0.040 vs. 2.30 (2.65-4.33) with p = 0.018), (Fig. 1). Over multiple logistic regression nlysis, it ws concluded y oserve the finl model of regression, only the presence of MetS remined ssocited with Hyperuricemi mong oese dolescents. It ws exmined tht, mong oese dolescents with MetS, the possiility of hving incresed UA levels ws lmost four times higher thn mong oese dolescents without the presence of metolic syndrome; s indicted y the results of the Hosmer nd Lemeshow test, the model presented good fit (Tle 3). DISCUSSION The prevlence of MetS in our results ws higher in mles compre to femles. This result is consistent with Irnin study mong children nd dolescents tht showed the prevlence of MetS mong mle sujects ws 11% vs. femle 7% (Rshidi et l., 2014). The higher numer of MetS mong mle oese dolescents ws lso found in previous studies (Sewyricker et l., 2013; Evi-Viscrr et l., 2013). This study hve lso presented tht UA levels incresed with the numer of the MetS components. The result of this study confirms previous result tht the prevlence of higher UA levels ws higher in the dolescents with MetS (Crdoso et l., 2013) nd it confirmed tht oese dolescents with MetS hd higher risk to Hyperuricemi thn without MetS. Consistent with Pcifico et l. (2009) demonstrted the ssocition etween MetS with UA levels mong children nd dolescents (Pcifico et l., 2009). The difference etween our results nd Pcifico et l (2009) is in the sujects of study. Our study sujects ws only oese dolescents nd it showed tht the prevlence of MetS with hyperuricemi mong dolescents ws Tle 1: Wist circumference, neck circumference, lood pressure nd iochemicl prmeters etween gender mong 81 oese dolescents Prmeters Mles (N = 41) Femles (N = 40) Wist circumference (WC) 98.58±13.26 89.28±10.24 Neck circumference (NC) 38.38±2.70 34.08±2.07 Systolic Blood Pressure 125 (100-160) 112.5 (90-140) Distolic Blood Pressure 85 (80-90) 80 (70-90) Triglyceride (mg/dl) 83 (57-296) 81.5 (54-130) HDL Cholesterol (mg/dl) 35 (27-49) 35 (25-49) Fsting lood glucose (mg/dl) 92 (82-110) 92.5 (78-108) Uric cid levels (mg/dl) 7.48±2.30 6.19±1.53 Dt ws presented s men±sd (the Kolmogorof-Smirnoff p > 0.05). Dt ws presented s medin (minimum-mximum) (the Kolmogorof- Smirnoff p vlue<0.05) Fig. 1: Men of uric cid level etween risk fctors of metolic syndrome 35.8%, slightly lower compre to 41.6% mong children with MetS (Pcifico et l., 2009), ut higher thn Crdoso et l. (2013). According to previous study there ws n interconnected mechnisms etween MetS, proinflmmtory rection nd dietes tht my effect to increse UA levels (Bldwin et l., 2011; Li et l., 2013). It ws concluded tht underlying fctor of insulin normlities (e.g. insulin resistnce) triggered delivernce of nitric oxide (NO) from endothelil cells. Oesity s underlying risk fctor of MetS ws decresing diponectin nd incresed inflmmtory response in dipose tissue. It will increse Monocyte Chemotctic Protein-1 (MCP-1) which hs n importnt role in insulin resistnce development. Hving sid tht, uric cid hs reported lso increse MCP-1 (Knd et l., 2006). Uric cid is the finl product of purine in humns nd in norml vlue it hs the strength to protect cell memrne from lipid oxidtion. Hyperuricemi is now commonly ssocited with fctors in MetS e.g., centrl oesity, hypertriglyceridemi, hypertension nd hyperglycemi (Xu et l., 2014). The correltion etween the concentrtion of uric cid with dominl oesity, insulin resistnce, hypertension nd dyslipidemi re complex nd i-directionl (Li et l., 2013). Pcifico et l. (2009) lso showed significnt correltion etween uric cid with components of the metolic syndrome. Uric cid concentrtions were significntly higher in 240
Pk. J. Nutr., 15 (3): 238-243, 2016 Tle 2: Gender, nthropometric, clinicl nd iochemicl vriles ccording to uric cid serum levels mong 81 oese dolescents ----------------- Uric cid ctegorize ------------------ Vriles Hyperuricemi (n = 55) Norml (n = 26) PR (95% CI) P Gender Mle 32 (39.5) 9 (11.1) 2.63 (0.99-6.93) 0.048 Femle 23 (28.4) 17 (21.0) WC Incresed 32 (39.5) 12 (14.8) 1.62 (0.63-4.15) 0.310 Norml 23 (28.4) 14 (17.3) NC Incresed 39 (48.1) 14 (17.3) 2.09 (0.79-5.49) 0.132 Norml 16 (19.8) 12 (14.8) SBP SBP>125 mmhg 20 (34.7) 8 (9.9) 1.29 (0.47-3.48) 0.621 SBP<125 mmhg 35 (43.2) 18 (22.2) DBP DBP>75 mmhg 30 (37.0) 14 (17.3) 1.03 (0.40-2.62) 0.953 DBP<75 mmhg 25 (30.9) 12 (14.8) TG Altered 14 (17.3) 0 (0.0) - - Norml 41 (50.6) 26 (32.1) HDL-c Low 39 (48.1) 18 (22.2) 1.08 (0.39-2.99) 0.877 Norml 16 (19.8) 8 (9.9) FBG Altered 0 (0.0) 1 (1.2) - - Norml 55 (67.9) 25 (30.9) MetS Present 29 (35.8) 5 (6.2) 4.68 (1.54-14.21) 0.004 Asent 26 (32.1) 21 (25.9) CI: Confidence intervl, WC: Wist circumference, NC: Neck circumference, PR: Prevlence rtio, SBP: Systolic lood pressure, DBP: Distolic lood pressure, TG: Triglycerides, HDL-c: High density lipoprotein, MetS: Metolic Syndrome. Chi Squre p-vlues Tle 3: Adjusted odds rtio (95% confidence intervl) of ltertions in uric cid in 81 oese dolescents Dependent Vriles Adjusted OR Adjusted p-vlue (95% CI) p-vlue hosmer nd lemeshow Hyperuricemi Gender (mle vs. femle) 1.92 0.209 (0.69-4.39) 0.697 Presence of metolic syndrome 3.97 0.018 (1.27-12.41) Logistic regression model fit (p-vlue Hosmer nd Lemeshow>0.05), The presence of metolic syndrome hs een risked to Hyperuricemi 3.97 higher thn without metolic syndrome ccordnce with the numer of risk fctors tht exist in the metolic syndrome (Pcifico et l., 2009). Uric cid levels could e developed s sensitive mrker of metolic syndrome (Zhng et l., 2013). Incresing of UA levels dministered low-degree inflmmtion, insulin resistnce nd metolic syndrome y MCP-1 ctivtion nd decresed in diponectin. MCP-1 is n inflmmtory cytokine tht might e over expression in metolic syndrome induced y oxidtive stress. Oesity ws contriuted to dipose tissue oxidtive stress (Bldwin et l., 2011). Previous study in vivo nd in vitro conducted y Zhu et l. (2014) showed mechnisms of hyperuricemi impired insulin sensitivity through direct mechnisms. Hyperuricemi could directly inhiited insulin lert to liver nd ft tissue. It promoted oxidtive stress s the importnt role in mechnism of hyperuricemi-insulin resistnce (Zhu et l., 2014). In future, prevlence of the MetS in Indonesin dolescents is estimted to increse long with the incresing prevlence of oesity nd lifestyle chnges, where it would increse the incidence of insulin resistnce. Furthermore, it is known tht there is direct reltionship etween hyperuricemi nd insulin resistnce. Hyperuricemi induced insulin resistnce s mrker of the MetS with vrious consequences (Mnzto, 2007). On histologic exmintion of kidney tissue found drmtic increse in renl prenchyml infiltrtion y mcrophges tht showed high levels of uric cid. Incresed levels of uric cid tht hs triggered inflmmtion of the kidneys, ctivting the reninngiotensin system nd reduce the production of NO which re ll importnt pthwys the uric-cid-medited hypertension (Nkgw et l., 2006). Incresing of uric cid ws n independent risk fctor in dietes mellitus oth in men nd women, furthermore met-nlysis reported tht high levels of uric cid s n independent risk fctor for metolic component in middle ge (Lv et l., 2013). Likewise, hyperinsulinemi nd hyperuricemi hve n influence one to nother. However in this study, we did not investigte HOMA IR due to limittion of resources. 241
Pk. J. Nutr., 15 (3): 238-243, 2016 Conclusion: Exmintion of uric cid should e considered lthough without ny signs nd symptoms of gout ecuse UA is modifile risk fctor of metolic syndrome. ACKNOWLEDGEMENT This study ws supported y Reserch Grnt Fculty of Medicine, Diponegoro University Semrng, Indonesi Ministry of Reserch, Technology nd Higher Eduction. Author disclosure sttement: The uthors declre no conflict of interest. REFERENCES Aswthpp, J., S. Grg, K. Kutty nd V. Shnkr, 2013. Neck circumference s n nthropometric mesure of oesity in dietics. North Am. J. Med. Sci., 5: 28. Bldwin, W., S. McRe, G. Mrek, D. Wymer nd V. Pnnu et l., 2011. Hyperuricemi s meditor of the proinflmmtory endocrine imlnce in the dipose tissue in murine model of the metolic syndrome. Dietes, 60: 1258-1269. Crdoso, A.S., N.C. Gonzg, C.C. Medeiros nd D.F. de Crvlho, 2013. Assocition of uric cid levels with components of metolic syndrome nd nonlcoholic ftty liver disese in overweight or oese children nd dolescents. J. Peditric, 89: 412-418. Evi-Viscrr, M.L., E.R. Rode-Montero, E. Apolinr- Jimenez nd S. Quintn-Vrgs, 2013. Metolic syndrome nd its components mong oese (BMI> 95th) Mexicn dolescents. Endocrinol. Connect, 2: 208-215. Feig, D.I., D.H. Kng nd R.J. Johnson, 2008. Uric cid nd crdiovsculr risk. N. Eng. J. Med., 359: 1811-1821. Ferretti, R.L., I.P. Cintr, M.A. Pssos, G.L. Ferrri nd M. Fiserg, 2015. Elevted neck circumference nd ssocited fctors in dolescents. BMC Pulic Helth, 15: 208. Grundy, S.M., H.B. Brewer, J.I. Cleemn, S.C. Smith nd C. Lenfnt, 2004. Definition of metolic syndrome report of the Ntionl Hert, Lung nd Blood Institute/Americn Hert Assocition Conference on scientific issues relted to definition. Circultion, 109: 433-438. Indonesin Ministry of Helth, 2013. Bsic Helth Reserch in Yer 2013, Report. Knellis, J. nd D.H. Kng, 2005. Uric cid s meditor of endothelil dysfunction, inflmmtion nd vsculr disese. In Seminrs in nephrology Jnury 2015. WB Sunders, pp: 39-42. Klein, S., D.B. Allison, S.B. Heymsfield, D.E. Kelley, R.L. Leiel, C. Nons nd R. Khn, 2007. Wist circumference nd crdiometolic risk: consensus sttement from shping Americ's helth: Assocition for Weight Mngement nd Oesity Prevention; NAASO, the Oesity Society; the Americn Society for Nutrition nd the Americn Dietes Assocition. Oes., 15: 1061-1067. Knd, H., S. Ttey, Y. Tmori, K. Kotni nd K. I. His et l., 2006. MCP-1 contriutes to mcrophge infiltrtion into dipose tissue, insulin resistnce nd heptic stetosis in oesity. J. Clin. Inves., 116: 1494. Lloyd, L.J., S.C. Lngley-Evns nd S. McMullen, 2012. Childhood oesity nd risk of the dult metolic syndrome: systemtic review. Int. J. Oes., 36: 1-11. Lippi, G., M. Montgnn, M. Frnchini, E.J. Fvloro nd G. Trgher, 2008. The prdoxicl reltionship etween serum uric cid nd crdiovsculr disese. Clin. Chim. Act, 392: 1-7. Li, C., M.C. Hsieh nd S.J. Chng, 2013. Metolik syndrome, dietes nd hiperuricemi. Current Opin Rheumtology, 25: 210-216. Lv, Q., X.F. Meng, F.F. He, S. Chen, H. Su, J. Xiong, P. Go, X.J. Tin, J.S. Liu, Z.H. Zhu, K. Hung nd C. Zhng, 2013. High serum uric cid nd incresed risk of type 2 dietes: A systemic review nd met-nlysis of prospective cohort studies. PLOS ONE, 8: 1-7. McGill, H.C., C.A. McMhn, E.E. Herderick, G.T. Mlcom nd R.E. Trcy et l., 2000. Origin of therosclerosis in childhood nd dolescence. Am. J. Clin. Nutr., 72: 1307s-1315s. Mnzto, E., 2007. Uric cid: n old ctor for new role. Intern. Emerg. Med., 2: 1-2. Nghm, K., K. Iseki, T. Inoue, T. Toum, Y. Ikemiy nd S. Tkishit, 2004. Hyperuricemi nd crdiovsculr risk fctor clustering in screened cohort in Okinw, Jpn. Hypertension Res., 27: 227-233. Nkgw, T., D.H. Kng, D. Feig, L.G. Snchez-Lozd nd T.R. Srinivs et l., 2006. Unerthing uric cid: n ncient fctor with recently found significnce in renl nd crdiovsculr disese. Kidney Int., 69: 1722-1725. Pcifico, L., V. Cntisni, C. Anni, E. Boniuto, F. Mrtino, R. Pscone nd C. Chies, 2009. Serum uric cid nd its ssocition with metolic syndrome nd crotid therosclerosis in oese children. Eur. J. Endocrinol., 160: 45-52. Rshidi, H., S.P. Pymi, S.M. Ltifi, M. Krndish nd A.M. Aleli, 2014. Prevlence of metolic syndrome nd its correlted fctors mong children nd dolescents of Ahvz ged 10-19. J. Dietes Met. Disord., 13: 53. Sewyricker, L.E., M.A.R. Antonio, R.T. Mendes, A.D.A. Brros Filho nd M.P. Zmon, 2013. Metolic syndrome in oese dolescents: wht is enough?. Rev. Assoc. Med. Brs., 59: 64-71. Thmn, R.G. nd G.P. Aror, 2013. Metolic Syndrome: Definition nd pthophysiology the discussion goes on. J. Phys. nd Phrmco., 3: 48-56. 242
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