AML 12 is a recently established differentiated, non-transformed hepatocyte cell line derived from mice transgenic for transforming growth factor alpha (Wu et al. (1994) Proc. Natl. Acad. Sci. 91, 674-678). The ability of these cells to take up [3H]cholesterol-labeled in vivo-generated chylomicron remnants, as well as [3H]cholesterol-labeled chylomicrons treated with hepatic lipase in vitro was investigated. Both types of lipoprotein particles were taken up by the AML hepatocytes at a much faster rate than intact chylomicrons, and in a saturable and specific manner. Chylomicrons treated with hepatic lipase in vitro competed with in vivo-generated chylomicron remnants for uptake by the AML hepatocytes, and the uptake of both types of lipoproteins was inhibited by lactoferrin, suggesting that they share the same process of cellular recognition and uptake. It is suggested that hepatic lipase-treated chylomicrons may be valuable in studies aimed at gaining a better understanding of the processes involved in the hepatic recognition and uptake of chylomicron remnants. AML hepatocytes, which can be maintained as replicating, untransformed, and differentiated under standard culture conditions, may be useful and practical for such studies.
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http://dx.doi.org/10.1016/0005-2760(95)00008-z | DOI Listing |
J Clin Med
September 2024
Glycation, Oxidation and Disease Laboratory, Touro University California, Vallejo, CA 94592, USA.
Over 50% of patients who take statins are still at risk of developing atherosclerotic cardiovascular disease (ASCVD) and do not achieve their goal LDL-C levels. This residual risk is largely dependent on triglyceride-rich lipoproteins (TRL) and their remnants. In essence, remnant cholesterol-rich chylomicron (CM) and very-low-density lipoprotein (VLDL) particles play a role in atherogenesis.
View Article and Find Full Text PDFArterioscler Thromb Vasc Biol
October 2024
Department of Medicine, Mike and Valeria Rosenbloom Centre for Cardiovascular Prevention, McGill University Health Centre, Montreal, Quebec, Canada (S.B., K.M.P., J.C., L.D., G.T., A.D.S.).
Background: Recent observational and Mendelian randomization analyses have reported significant effects of VLDL-C (very-low density lipoprotein cholesterol) on risk that is independent of ApoB (apolipoprotein B). We aim to determine the independent association of VLDL-C and ApoB with the risk of new onset cardiovascular events in the UK Biobank and Framingham Heart Study cohorts.
Methods: We included 294 289 UK Biobank participants with a median age of 56 years, 42% men, and 2865 Framingham Heart Study participants (median age, 53 years; 47% men).
J Atheroscler Thromb
July 2024
Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Front Endocrinol (Lausanne)
February 2024
Glycation, Oxidation and Disease Laboratory, Department of Research, Touro University California, Vallejo, CA, United States.
Since statins have had such tremendous therapeutic success over the last three decades, the field of atherosclerosis has become somewhat LDL-centric, dismissing the relevance of triglycerides (TG), particularly chylomicrons, in atherogenesis. Nonetheless, 50% of patients who take statins are at risk of developing atherosclerotic cardiovascular disease (ASCVD) and are unable to achieve their goal LDL-C levels. This residual risk is mediated, in part by triglyceride rich lipoproteins (TRL) and their remnants.
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