{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,19]],"date-time":"2026-03-19T12:27:19Z","timestamp":1773923239264,"version":"3.50.1"},"reference-count":24,"publisher":"Walter de Gruyter GmbH","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2018,6,27]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec id=\"j_dmpt-2017-0013_s_999_w2aab2b8b1b1b7b1aab1c16b1Aa\">\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>Abdominal adiposity has a central role in developing insulin resistance (IR) by releasing pro-inflammatory cytokines. Patients with metabolic syndrome (MS) have higher values of homocysteine. Hyperhomocysteinemia correlates with IR, increasing the oxidative stress. Oxidative stress causes endothelial dysfunction, hypertension and atherosclerosis. The objective of the study was to examine the correlation of homocysteine with siMS score and siMS risk score and with other MS co-founding factors.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"j_dmpt-2017-0013_s_998_w2aab2b8b1b1b7b1aab1c16b2Aa\">\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>\n                      The study included 69 obese individuals (age over 30, body mass index [BMI] &gt;25 kg\/m\n                      <jats:sup>2<\/jats:sup>\n                      ), classified into two groups: I-with MS (33 patients); II-without MS (36 patients). Measurements included: anthropometric parameters, lipids, glucose regulation parameters and inflammation parameters. IR was determined by homeostatic model assessment for insulin resistance (HOMA-IR). ATP III classification was applied for diagnosing MS. SiMS score was used as continuous measure of metabolic syndrome.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"j_dmpt-2017-0013_s_997_w2aab2b8b1b1b7b1aab1c16b3Aa\">\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      A significant difference between groups was found for C-reactive protein (CRP) (p&lt;0.01) apolipoprotein (Apo) B, HOMA-IR and acidum uricum (p&lt;0.05). siMS risk score showed a positive correlation with homocysteine (p=0.023), while siMS score correlated positively with fibrinogen (p=0.013), CRP and acidum uricum (p=0.000) and homocysteine (p=0.08). Homocysteine correlated positively with ApoB (p=0.036), HbA\n                      <jats:sub>1c<\/jats:sub>\n                      (p=0.047), HOMA-IR (p=0.008) and negatively with ApoE (p=0.042).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"j_dmpt-2017-0013_s_996_w2aab2b8b1b1b7b1aab1c16b4Aa\">\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>Correlation of siMS score with homocysteine, fibrinogen, CRP and acidum uricum indicates that they are co-founding factors of MS. siMS risk score correlation with homocysteine indicates that hyperhomocysteinemia increases with age. Hyperhomocysteinemia is linked with genetic factors and family nutritional scheme, increasing the risk for atherosclerosis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1515\/dmpt-2017-0013","type":"journal-article","created":{"date-parts":[[2018,4,6]],"date-time":"2018-04-06T03:41:47Z","timestamp":1522986107000},"page":"99-103","source":"Crossref","is-referenced-by-count":11,"title":["Homocysteine is the confounding factor of metabolic syndrome-confirmed by siMS score"],"prefix":"10.1515","volume":"33","author":[{"given":"Branko","family":"Sre\u0107kovi\u0107","sequence":"first","affiliation":[{"name":"Clinical Center Be\u017eanijska Kosa , 11000 Belgrade , Serbia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ivan","family":"Soldatovic","sequence":"additional","affiliation":[{"name":"Institute for Medical Statistics and Informatics , Belgrade , Serbia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Emina","family":"Colak","sequence":"additional","affiliation":[{"name":"Institute of Medical Biochemistry, Clinical Center of Serbia , Belgrade , Serbia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Igor","family":"Mrdovic","sequence":"additional","affiliation":[{"name":"Clinic for Cardiovascular Diseases, Emergency Center , Belgrade , Serbia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mirjana","family":"Sumarac-Dumanovic","sequence":"additional","affiliation":[{"name":"Clinic for Endocrinology, Diabetes and Metabolic Diseases, Clinical Center of Serbia and Faculty of Medicine , University of Belgrade , Belgrade , Serbia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hristina","family":"Janeski","sequence":"additional","affiliation":[{"name":"University Children\u2019s Hospital , Belgrade , Serbia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nenad","family":"Janeski","sequence":"additional","affiliation":[{"name":"Clinical Center Zemun , Belgrade , Serbia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jasna","family":"Gacic","sequence":"additional","affiliation":[{"name":"Clinical Center Be\u017eanijska Kosa , Belgrade , Serbia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Vesna","family":"Dimitrijevic-Sreckovic","sequence":"additional","affiliation":[{"name":"Clinic for Endocrinology, Diabetes and Metabolic Diseases, Clinical Center of Serbia and Faculty of Medicine , University of Belgrade , Belgrade , Serbia"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"374","published-online":{"date-parts":[[2018,4,6]]},"reference":[{"key":"2025121207100438244_j_dmpt-2017-0013_ref_001_w2aab2b8b1b1b7b1ab2b1b1Aa","doi-asserted-by":"crossref","unstructured":"Jacques PF, Bostom AG, Williams RR, Ellison RC, Eckfeldt JH, Rosenberg IH, et al. 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