Simon-Pierre Noël
McGill University
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Featured researches published by Simon-Pierre Noël.
Journal of Clinical Investigation | 1979
Simon-Pierre Noël; Laurence Wong; Peter J. Dolphin; Ladislav Dory; David Rubinstein
Rats maintained on a high-fat diet supplemented with propylthiouracil develop a hypercholesterolemia, an increased serum level of apolipoprotein (apo) E, abnormal very low density lipoproteins (VLDL) and low density lipoproteins (LDL), and a fatty liver which contains cholesterol ester as its major lipid. The fatty liver secretes apoE into a recirculating perfusate at a significantly higher rate and produces cholesterol ester-rich, apoC-deficient VLDL with slower electrophoretic mobility than the triacylglycerol-rich VLDL produced by perfused normal livers. LDL, secreted in significant quantities by the perfused fatty liver, but not by the normal liver, is also cholesterol rich and contains apoE as well as apoB. The incorporation of [(3)H]leucine into apoVLDL and apoLDL secreted by the livers of the hypercholesterolemic animals and the apoVLDL secreted by the normal liver corresponds to the pattern visualized when the apoproteins are separated by polyacrylamide gel electrophoresis. Similar patterns are noted when non-recirculating perfusates are studied. These results indicate that the cholesterol ester-rich, apoC-deficient VLDL and the apoE-containing LDL found in the serum of hypercholesterolemic rats are not solely catabolic remnants of VLDL and chylomicrons but are secreted by the liver. Separation of the perfusate lipoproteins by agarose gel filtration revealed that most of the apoE secreted by the livers of hypercholesterolemic rats is found in the VLDL and LDL, whereas apoE secreted by the normal livers is distributed equally between VLDL, high density lipoproteins, and a low molecular weight fraction which corresponds to the virtually delipidated apoprotein. Thus the distribution of apoE among the lipoprotein fractions may be related to the total amount of cholesterol being transported in the circulation.
Biochemical and Biophysical Research Communications | 1975
Simon-Pierre Noël; Peter J. Dolphin; David Rubinstein
Summary An in vitro model for the study of the catabolism of chylomicrons is suggested and characterized. The model utilizes the ability of perfused rat hearts to hydrolyze triglycerides of chylomicrons obtained from rat thoracic ducts. The resulting remnants were re-isolated and perfused through rat livers where the remnant lipid and protein was rapidly removed. In contrast intact chylomicrons were taken up by perfused liver to a limited extent. The remnants produced by cardiac perfusion contained a decreased percent of triglycerides and apoproteins C-2 and C-3, with a relative increase primarily in diglycerides and, to a lesser extent, monoglycerides and cholesterol. Most of the 125I-labelled remnant protein lost during hepatic perfusion was recovered in the tissue. The model thus simulated many of the known characteristics of chylomicron catabolism in vivo .
Cellular and Molecular Life Sciences | 1982
H. Lee; Simon-Pierre Noël; E. A. Hosein; David Rubinstein
Chronic alcohol feeding of a low fat diet for 5 weeks led to a slightly raised though statistically non-significant high density liproprotein cholesterol/apoB containing lipoprotein cholesterol ratio in both the fasting rat serum as well as the secretory products of the isolated perfused liver.
Journal of Lipid Research | 1974
Simon-Pierre Noël; David Rubinstein
Journal of Lipid Research | 1987
Paul D. Roach; M Zollinger; Simon-Pierre Noël
Journal of Biological Chemistry | 1986
Louise Brissette; Paul D. Roach; Simon-Pierre Noël
Journal of Lipid Research | 1987
Paul D. Roach; Simon-Pierre Noël
Journal of Lipid Research | 1985
Paul D. Roach; Simon-Pierre Noël
Biochemistry and Cell Biology | 1981
Simon-Pierre Noël; David Rubinstein
Biochemistry and Cell Biology | 1984
Louise Brissette; Simon-Pierre Noël