Plasma low density lipoprotein composition in relation to atherosclerosis in nutritionally defined Vervet monkeys

Benadé, A. J. S.; Fincham, J.E.; Smuts, Cornelius M.; Tung, Marie Thérèse Lai; Chalton, D. O.; Kruger, M.; Weight, M.J.; Daubitzer, Annette K.; Tichelaar, H.Y.

doi:10.1016/0021-9150(88)90202-x

Cited by 27 publications

(20 citation statements)

References 33 publications

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“…Geelen et al (204) reported an increase of plasma SM in rats fed cholesterol. Benade et al (205) fed an atherogenic diet consisting entirely of normal foods to female vervet monkeys for 4 years as well as a more prudent control diet. The LDL cholesterol was 3-fold higher and the SM was 2-fold higher with the atherogenic diet as a result of the increased number of LDL particles.…”

Section: Effects Of Dietmentioning

confidence: 99%

Absorption and lipoprotein transport of sphingomyelin

Nilsson

Duan

2006

Journal of Lipid Research

227

201

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Dietary sphingomyelin (SM) is hydrolyzed by intestinal alkaline sphingomyelinase and neutral ceramidase to sphingosine, which is absorbed and converted to palmitic acid and acylated into chylomicron triglycerides (TGs). SM digestion is slow and is affected by luminal factors such as bile salt, cholesterol, and other lipids. In the gut, SM and its metabolites may influence TG hydrolysis, cholesterol absorption, lipoprotein formation, and mucosal growth. SM accounts for z20% of the phospholipids in human plasma lipoproteins, of which two-thirds are in LDL and VLDL. It is secreted in chylomicrons and VLDL and transferred into HDL via the ABCA1 transporter. Plasma SM increases after periods of large lipid loads, during suckling, and in type II hypercholesterolemia, cholesterol-fed animals, and apolipoprotein E-deficient mice. SM is thus an important amphiphilic component when plasma lipoprotein pools expand in response to large lipid loads or metabolic abnormalities. It inhibits lipoprotein lipase and LCAT as well as the interaction of lipoproteins with receptors and counteracts LDL oxidation. The turnover of plasma SM is greater than can be accounted for by the turnover of LDL and HDL particles. Some SM must be degraded via receptor-mediated catabolism of chylomicron and VLDL remnants and by scavenger receptor class B type I receptor-mediated transfer into cells. Sphingomyelin (SM) in mammalian cells is colocalized with cholesterol mainly in the plasma membrane and in lysosomal and Golgi membranes. It interacts strongly with cholesterol, and the regulation of SM and cholesterol metabolism are in part coordinated (1, 2). In plasma lipoproteins, SM is the second most abundant polar lipid after phosphatidylcholine (PC). The size of the plasma lipoprotein SM pool in humans is 1-1.5 g, of which approximately two-thirds are in apolipoprotein B (apoB)-containing triglyceride (TG)-rich lipoproteins and LDL. The SM content in most extraneural tissues is 1-2 g/kg. Factors regulating plasma SM concentration have received little attention. It was early shown that the level of SM is increased in hypercholesterolemia and that SM-rich lipoproteins accumulate in arteriosclerotic lesions (3-5). Plasma SM is thus a risk factor for ischemic heart disease (6), and the apoE-deficient (apoE 2/2 ) mouse, which accumulates SM-rich remnant particles in blood (7), has emerged as an important model for studying the role of SM in atherogenesis. The effects of lipoprotein SM in the arterial wall during atherogenesis may be related both to the modification of lipoproteins and to the generation of sphingolipid messengers (i.e., ceramide, ceramide-1-phosphate, sphingosine, and sphingosine-1-phosphate) initiated by SM hydrolysis (8-10). The role of SM metabolites in cell signaling has been the subject of several recent reviews (11)(12)(13)(14)(15)(16). Sphingolipid signals are triggered by numerous stimuli and mediate effects on cell growth and apoptosis and on the activities of inflammatory cells that may be pathogenic as well as protect...

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Section: Effects Of Dietmentioning

confidence: 99%

Absorption and lipoprotein transport of sphingomyelin

Nilsson

Duan

2006

Journal of Lipid Research

227

201

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“…The fatty acid contents of the oils were present as TGs and were checked by analysis 42 five times during the experiment; eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in the FO averaged 22.9±1.3% and 7.4±0.7%, respectively, of the total fatty acids. The SO contained 65.6±2.3% linoleic acid.…”

Section: Design Of Experiment Oil Supplements Diets and Quality Comentioning

confidence: 99%

“…The patties were analyzed for fat, cholesterol, and fatty acid content by described methods. 42 In addition, raw apple averaging 52.5 ±6.4 g and vitamins C (40 mg), D ? (200 IU), and folic acid (500 fig) were provided daily.…”

Section: Design Of Experiment Oil Supplements Diets and Quality Comentioning

confidence: 99%

“…Since a major source of FO from Atlantic pilchards (Sardinops oscellata) is available commercially as a food supplement, the experiment tested for antiatherogenic effects of this oil when combined with a proven AD 41 - 42 and for an increased effect by changing to a therapeutic diet (TD) with FO added. Polyunsaturates supplied by the FO were controlled by sunflower (Helianthus annuus) seed oil (SO) rich in linoleic acid in the same diets fed to matched groups.…”

Section: Design Of Experiment Oil Supplements Diets and Quality Comentioning

confidence: 99%

“…Any effects due to FO were gauged against those of a dietary treatment known to be antiatherogenic in the model. 41 " 43 Dietary treatments were not loaded excessively with saturated fat and cholesterol to accelerate ath-erogenesis because this might have distorted the results, 42 - 44 and compliance was confirmed.…”

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confidence: 99%

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