siMS score- method for quantification of metabolic syndrome, confirms co-founding factors of metabolic syndrome

siMS评分——一种用于量化代谢综合征的方法,证实了代谢综合征的共同致病因素。

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Abstract

Background: Adipose tissue is a dynamic endocrine organ, a highly active metabolic tissue, and an important source of cytokines. Inflammatory factors play an important role in visceral obesity associated with insulin resistance (IR), metabolic syndrome (MS), hypertension, non-alcoholic fatty liver disease (NAFLD), diabetes mellitus type 2 (DM2), endothelial dysfunction (ED) and atherosclerosis. Objectives: To examine corelation of siMS score, as a quantification method for metabolic syndrome (MS), with insulin resistance, glucoregulation parameters, as with other co-founding factors of MS, inflammation and thrombosis factors, microalbuminuria, uric acid, fatty liver index (FLI) and homocysteine. Methods: The study included 451 obese individuals with pre-metabolic syndrome (pre-MS) and MS (age 16-75, body mass index (BMI) > 25kg/m(2)) classified into two groups: I-age 10-30 (167 patients); II-age 31-75 (284 patients). International Diabetes Federation (IDF) classification was applied for diagnosing metabolic syndrome. Patients with less than three criteria indicated below were considered pre-metabolic syndrome. siMS risk score was used. Results: siMS score increased with age: I-3.03 ± 0.87, II-3.27 ± 0.90. siMS score correlated with associated factors of MS: hyperinsulinemia and IR, ALT, gama-GT, FLI, uric acid in both groups and CRP (p < 0.01) in group I. Correlations in II group: siMS score with PAI-1 (p = 0.01), microalbuminuria (p = 0.006), homocysteine ​​(p = 0.076). Conclusion: Correlation of siMS score with HOMA-IR confirmed that hyperinsulinism and insulin resistance are in the basis of MS. Correlation of siMS score with parameters of NAFLD, CRP, PAI-1, uric acid, microalbuminuria and homocysteine indicates that they are significant co-founding factors of MS. Correlation of siMS score with PAI-1, microalbuminuria, homocysteine, indicates higher risk for progression of endothelial dysfunction and atherosclerosis with age.

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