Zareen M Farukhi1, Olga V Demler1, Michael P Caulfield2, Krishnaji Kulkarni3, Jay Wohlgemuth2, Michael Cobble3, Heike Luttmann-Gibson4, Chunying Li5, John R Nelson6, Nancy R Cook5, Julie E Buring5, Ronald M Krauss7, JoAnn E Manson5, Samia Mora8. 1. Center for Lipid Metabolomics, Division of Preventive Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA; Division of Preventive Medicine, Brigham and Women's Hospital, Boston, MA, USA. 2. Quest Diagnostics, San Juan Capistrano, CA, USA. 3. VAP Diagnostics Laboratory, Birmingham, AL, USA. 4. Division of Preventive Medicine, Brigham and Women's Hospital, Boston, MA, USA; Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA. 5. Division of Preventive Medicine, Brigham and Women's Hospital, Boston, MA, USA. 6. California Cardiovascular Institute, Fresno, CA, USA. 7. Children's Hospital Oakland Research Institute, Oakland, CA, USA. 8. Center for Lipid Metabolomics, Division of Preventive Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA; Division of Preventive Medicine, Brigham and Women's Hospital, Boston, MA, USA; Division of Cardiovascular Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. Electronic address: smora@bwh.harvard.edu.
Abstract
BACKGROUND: Elevated postprandial triglycerides reflect a proatherogenic milieu, but underlying mechanisms are unclear. OBJECTIVE: We examined differences between fasting and nonfasting profiles of directly measured lipoprotein size and subfractions to assess if postprandial triglycerides reflected increases in very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL) and remnants, or small dense lipid depleted LDL (sdLDL) particles. METHODS: We conducted a cross-sectional analysis of 15,397 participants (10,135 fasting; 5262 nonfasting [<8 hours since last meal]) from the VITamin D and OmegA-3 TriaL. Baseline cholesterol subfractions were measured by the vertical auto profile method and particle subfractions by ion mobility. We performed multivariable linear regression adjusting for cardiovascular and lipoprotein-modifying risk factors. RESULTS: Mean age (SD) was 68.0 years (±7.0), with 50.9% women. Adjusted mean triglyceride concentrations were higher nonfasting by 17.8 ± 1.3%, with higher nonfasting levels of directly measured VLDL cholesterol (by 3.5 ± 0.6%) and total VLDL particles (by 2.0 ± 0.7%), specifically large VLDL (by 12.3 ± 1.3%) and medium VLDL particles (by 5.3 ± 0.8%), all P < .001. By contrast, lower concentrations of low density lipoprotein (LDL) and IDL cholesterol and particles were noted for nonfasting participants. sdLDL cholesterol levels and particle concentrations showed no statistically significant difference by fasting status (-1.3 ± 2.1% and 0.07 ± 0.6%, respectively, P > .05). CONCLUSIONS: Directly measured particle and cholesterol concentrations of VLDL, not sdLDL, were higher nonfasting and may partly contribute to the proatherogenicity of postprandial hypertriglyceridemia. These differences, although statistically significant, were small and may not fully explain the increased risk of postprandial hypertriglyceridemia.
BACKGROUND: Elevated postprandial triglycerides reflect a proatherogenic milieu, but underlying mechanisms are unclear. OBJECTIVE: We examined differences between fasting and nonfasting profiles of directly measured lipoprotein size and subfractions to assess if postprandial triglycerides reflected increases in very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL) and remnants, or small dense lipid depleted LDL (sdLDL) particles. METHODS: We conducted a cross-sectional analysis of 15,397 participants (10,135 fasting; 5262 nonfasting [<8 hours since last meal]) from the VITamin D and OmegA-3 TriaL. Baseline cholesterol subfractions were measured by the vertical auto profile method and particle subfractions by ion mobility. We performed multivariable linear regression adjusting for cardiovascular and lipoprotein-modifying risk factors. RESULTS: Mean age (SD) was 68.0 years (±7.0), with 50.9% women. Adjusted mean triglyceride concentrations were higher nonfasting by 17.8 ± 1.3%, with higher nonfasting levels of directly measured VLDL cholesterol (by 3.5 ± 0.6%) and total VLDL particles (by 2.0 ± 0.7%), specifically large VLDL (by 12.3 ± 1.3%) and medium VLDL particles (by 5.3 ± 0.8%), all P < .001. By contrast, lower concentrations of low density lipoprotein (LDL) and IDL cholesterol and particles were noted for nonfasting participants. sdLDLcholesterol levels and particle concentrations showed no statistically significant difference by fasting status (-1.3 ± 2.1% and 0.07 ± 0.6%, respectively, P > .05). CONCLUSIONS: Directly measured particle and cholesterol concentrations of VLDL, not sdLDL, were higher nonfasting and may partly contribute to the proatherogenicity of postprandial hypertriglyceridemia. These differences, although statistically significant, were small and may not fully explain the increased risk of postprandial hypertriglyceridemia.
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