Postprandial accumulation of chylomicrons and chylomicron remnants is determined by the clearance capacity.

[1]  N. Lundbom,et al.  Dual Metabolic Defects Are Required to Produce Hypertriglyceridemia in Obese Subjects , 2011, Arteriosclerosis, thrombosis, and vascular biology.

[2]  Jukka Westerbacka,et al.  Long‐TE 1H MRS suggests that liver fat is more saturated than subcutaneous and visceral fat , 2011, NMR in biomedicine.

[3]  F. Tinahones,et al.  Effect of apolipoprotein C3 and apolipoprotein A1 polymorphisms on postprandial response to a fat overload in metabolic syndrome patients. , 2010, Clinical biochemistry.

[4]  M. Jensen,et al.  Postabsorptive VLDL‐TG Fatty Acid Storage in Adipose Tissue in Lean and Obese Women , 2010, Obesity.

[5]  E. Ryan,et al.  Synthesis of specific fatty acids contributes to VLDL-triacylglycerol composition in humans with and without type 2 diabetes , 2009, Diabetologia.

[6]  A. Häkkinen,et al.  Acute suppression of VLDL1 secretion rate by insulin is associated with hepatic fat content and insulin resistance , 2007, Diabetologia.

[7]  N. Lundbom,et al.  Postprandial lipemia associates with liver fat content. , 2007, The Journal of clinical endocrinology and metabolism.

[8]  B. Nordestgaard,et al.  Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women. , 2007, JAMA.

[9]  P. Ridker,et al.  Fasting compared with nonfasting triglycerides and risk of cardiovascular events in women. , 2007, JAMA.

[10]  A. Häkkinen,et al.  Overproduction of large VLDL particles is driven by increased liver fat content in man , 2006, Diabetologia.

[11]  Bernt Wennberg,et al.  Overproduction of VLDL1 Driven by Hyperglycemia Is a Dominant Feature of Diabetic Dyslipidemia , 2005, Arteriosclerosis, thrombosis, and vascular biology.

[12]  Bernt Wennberg,et al.  A new combined multicompartmental model for apolipoprotein B-100 and triglyceride metabolism in VLDL subfractions Published, JLR Papers in Press, October 16, 2004. DOI 10.1194/jlr.M400108-JLR200 , 2005, Journal of Lipid Research.

[13]  R. Havel,et al.  Hepatic catabolism of remnant lipoproteins: where the action is. , 2004, Arteriosclerosis, thrombosis, and vascular biology.

[14]  K. Hermansen,et al.  Incremental area under response curve more accurately describes the triglyceride response to an oral fat load in both healthy and type 2 diabetic subjects. , 2003, Metabolism: clinical and experimental.

[15]  R. Zechner,et al.  Lipoprotein lipase: the regulation of tissue specific expression and its role in lipid and energy metabolism , 2002, Current opinion in lipidology.

[16]  A. Hamsten,et al.  Differences in postprandial concentrations of very-low-density lipoprotein and chylomicron remnants between normotriglyceridemic and hypertriglyceridemic men with and without coronary heart disease. , 1999, Metabolism: clinical and experimental.

[17]  M. Taskinen,et al.  Effects of insulin and acipimox on VLDL1 and VLDL2 apolipoprotein B production in normal subjects. , 1998, Diabetes.

[18]  J. Hokanson,et al.  Hypertriglyceridemia as a cardiovascular risk factor. , 1998, The American journal of cardiology.

[19]  A. V. van Beek,et al.  Preferential clearance of apoB-48-containing lipoproteins after heparin-induced lipolysis is modulated by lipoprotein lipase activity. , 1998, Journal of lipid research.

[20]  M. Taskinen,et al.  Postprandial elevation of ApoB-48-containing triglyceride-rich particles and retinyl esters in normolipemic males who smoke. , 1997, Arteriosclerosis, thrombosis, and vascular biology.

[21]  J. Hokanson,et al.  Plasma Triglyceride Level is a Risk Factor for Cardiovascular Disease Independent of High-Density Lipoprotein Cholesterol Level: A Metaanalysis of Population-Based Prospective Studies , 1996, Journal of cardiovascular risk.

[22]  L. Chambless,et al.  Association of postprandial triglyceride and retinyl palmitate responses with asymptomatic carotid artery atherosclerosis in middle-aged men and women. The Atherosclerosis Risk in Communities (ARIC) Study. , 1995, Arteriosclerosis, thrombosis, and vascular biology.

[23]  J. Björkegren,et al.  Quantification of postprandial triglyceride-rich lipoproteins in healthy men by retinyl ester labeling and simultaneous measurement of apolipoproteins B-48 and B-100. , 1995, Arteriosclerosis, thrombosis, and vascular biology.

[24]  A. Hamsten,et al.  Determination of apolipoproteins B-48 and B-100 in triglyceride-rich lipoproteins by analytical SDS-PAGE. , 1994, Journal of lipid research.

[25]  E. Johnson,et al.  Contribution of apoB-48 and apoB-100 triglyceride-rich lipoproteins (TRL) to postprandial increases in the plasma concentration of TRL triglycerides and retinyl esters. , 1993, Journal of lipid research.

[26]  G. Lewis,et al.  Effects of Acute Hyperinsulinemia on VLDL Triglyceride and VLDL ApoB Production in Normal Weight and Obese Individuals , 1993, Diabetes.

[27]  R. Havel,et al.  Relationships between the responses of triglyceride-rich lipoproteins in blood plasma containing apolipoproteins B-48 and B-100 to a fat-containing meal in normolipidemic humans. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[28]  K. Polonsky,et al.  Role of basal triglyceride and high density lipoprotein in determination of postprandial lipid and lipoprotein responses. , 1992, The Journal of clinical endocrinology and metabolism.

[29]  K. Polonsky,et al.  Fasting hypertriglyceridemia in noninsulin-dependent diabetes mellitus is an important predictor of postprandial lipid and lipoprotein abnormalities. , 1991, The Journal of clinical endocrinology and metabolism.

[30]  D. Porte,et al.  Evidence for a common, saturable, triglyceride removal mechanism for chylomicrons and very low density lipoproteins in man. , 1973, The Journal of clinical investigation.

[31]  Eric Boerwinkle,et al.  The Atherosclerosis Risk in Communities (ARIC) Study , 2011 .

[32]  A. Hamsten,et al.  Accumulation of large very low density lipoprotein in plasma during intravenous infusion of a chylomicron-like triglyceride emulsion reflects competition for a common lipolytic pathway. , 1996, Journal of lipid research.