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Background: The risk factors of Metabolic syndrome (Mets), primarily favors the development ofcardiometabolic alteration, type 2 diabetes, hypertension, and dyslipidemia leading to increase in morbidity.Life style and eating habits often increases the levels of Uric acid (UA) in circulation. Elevated UA &stress, exacerbates the pain and inflammation. The inflammatory response includes systemic increase incirculating inflammatory cytokines and acute phase protein, high sensitive C-reactive protein (hs-CRP).Adiponectin (ADI) a cytokines primarily secreted by adipocytes exerts antidiabetic, anti-inflammatory &cardioprotective effects. Thus the purpose of the study is to establish a link between Adiponectin, Uric acidand hs-CRP which may further be used in diagnosis and thus can positively reverse many of the adverseeffects of MetS.Material and Methods: Present study, an observational case-control study conducted on referred MetSpatients attending OPD at Chhatrapati Shivaji Subharti Hospital, Meerut. Data collected on previouslyvalidated questionnaire from 235 subjects (156 with MetS and 79 non-MetS) assessed for anthropometricmeasurements, diabetic profile, ADI, UA & hs-CRP were evaluated by standard established techniques.Results: The results obtained from Mets patients were compared with non-MetS subjects, where ADI wassignificantly lower (PIn Spearman’s rank correlation coefficient for the relationship between ADI and metabolic variables -ADI was positively correlated with age, diastolic blood pressure, total cholesterol, HDL-C& LDL-Cwhile negatively correlated with BMI, systolic blood pressure, fasting glucose, Triglyceride& VLDL-C.Serum hs-CRP levels were elevated with the increasing number of MetS components, being higher amongthose with > 2 components of MetS while adiponectin decreasing with the number of MetS components.Decreased levels were reported for ADI, whereas hs-CRP & UA levels were escalating.Conclusion: Higher levels of hs-CRP

Relationship between adiponectin & uric acid with inflammation in pathogenesis of metabolic syndrome