{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T02:37:58Z","timestamp":1788748678851,"version":"build-2803163510"},"reference-count":25,"publisher":"The Endocrine Society","issue":"1","license":[{"start":{"date-parts":[[2019,11,3]],"date-time":"2019-11-03T00:00:00Z","timestamp":1572739200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2020,1,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Context<\/jats:title>\n                  <jats:p>Calculated non\u2013high-density lipoprotein (HDL) cholesterol (non-HDLC) should selectively include cholesterol from atherogenic lipoproteins to be a reliable risk marker of cardiovascular disease. In hypertriglyceridemia (HTG), there is increased abundance of larger and less atherogenic triglyceride-rich lipoproteins (TRL), namely, larger very-low-density lipoproteins (VLDL), and chylomicrons.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Objective<\/jats:title>\n                  <jats:p>We aim to demonstrate that serum triglyceride (TG) level has a substantial impact on non-HDLC\u2019s ability to represent cholesterol from atherogenic lipoproteins, even though TG is not part of the calculation for non-HDLC.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Design<\/jats:title>\n                  <jats:p>Analysis of lipid profile data<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Settings<\/jats:title>\n                  <jats:p>Lipid Clinic patient cohort, and Biochemistry Laboratory patient cohort<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Patients or Other Participants<\/jats:title>\n                  <jats:p>7,492 patients in the Lipid Clinic cohort with baseline lipid profiles documented prior to starting lipid-lowering medications and 156,311 lipid profiles from The Ottawa Hospital Biochemistry Laboratory cohort.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Intervention<\/jats:title>\n                  <jats:p>None<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Main Outcome Measure<\/jats:title>\n                  <jats:p>Our modeling process includes derivation of TG-interval\u2013specific lipoprotein composition factor (LCF) for TRL, which represents the mass ratio of cholesterol to TG in TRL. A high LCF indicates that the TRLs are mainly the cholesterol-rich atherogenic remnant lipoproteins. A low LCF indicates that the TRLs are mainly the TG-rich larger VLDL and chylomicrons.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>As serum TG increases, there is progressive decline in the LCF for TRL, which indicates that the calculated non-HDLC level reflects progressive inclusion of cholesterol from larger TRL. This is shown in both cohorts.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>Calculated non-HDLC is influenced by TG level. As TG increases, non-HDLC gradually includes more cholesterol from larger TRL, which are less atherogenic than LDL and remnant lipoproteins.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1210\/jendso\/bvz010","type":"journal-article","created":{"date-parts":[[2019,11,3]],"date-time":"2019-11-03T06:56:01Z","timestamp":1572764161000},"source":"Crossref","is-referenced-by-count":9,"title":["Calculated Non-HDL Cholesterol Includes Cholesterol in Larger Triglyceride-Rich Lipoproteins in Hypertriglyceridemia"],"prefix":"10.1210","volume":"4","author":[{"given":"Cathy J","family":"Sun","sequence":"first","affiliation":[{"name":"Division of Endocrinology and Metabolism, Department of Medicine, University of Ottawa, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher","family":"McCudden","sequence":"additional","affiliation":[{"name":"Division of Biochemistry, Department of Pathology and Laboratory 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ECOGENE-21 Clinical and Translational Research Center, Chicoutimi, Quebec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8601-1055","authenticated-orcid":false,"given":"Teik C","family":"Ooi","sequence":"additional","affiliation":[{"name":"Division of Endocrinology and Metabolism, Department of Medicine, University of Ottawa, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"80","published-online":{"date-parts":[[2019,11,3]]},"reference":[{"issue":"11","key":"2021121116283073500_CIT0001","doi-asserted-by":"crossref","first-page":"1263","DOI":"10.1016\/j.cjca.2016.07.510","article-title":"2016 Canadian Cardiovascular Society Guidelines for the Management of Dyslipidemia for the Prevention of Cardiovascular Disease in the Adult","volume":"32","author":"Anderson","year":"2016","journal-title":"Can J 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