Structural and functional changes of rhesus serum low density lipoproteins during cycles of diet-induced hypercholesterolemia.

Fless, Gunther M.; Fischer-Dzoga, Katti; Juhn, Dawn J.; Bates, Sandra R.; Scanu, Angelo M.

doi:10.1161/01.atv.2.6.475

Cited by 40 publications

(9 citation statements)

References 25 publications

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“…5 Blood was collected frorti the femoral vein of monkeys anesthetized with ketamine and the serum was separated by centrifuging the blood at 4°C for 30 minutes at 1000 g.…”

Section: Methodsmentioning

confidence: 99%

“…5 HDL cholesterol was quantitated after the precipitation of the apo B containing lipoproteins from 1 ml serum with 40 IJL\ heparin (5 x 10 6 units/I) and 50 ^l 2 M MnCI 2 . 15 The cholesterol concentration of the supernatant was determined with the Liebermann-Burchard reaction using the Auto Analyzer II.…”

Section: Chemical Analysismentioning

confidence: 99%

“…5 These particles are structurally suited for uptake by B, and B, E receptors. At this stage, the HDL species finished their progressive shift to higher density and are relatively unimportant in comparison to LDL, p-VLDL, and pre-p-VLDL as vehicles for cholesterol transport.…”

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confidence: 99%

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Response of rhesus serum high density lipoproteins to cycles of diet-induced hypercholesterolemia.

Fless¹,

Juhn²,

Karlin³

et al. 1984

Arteriosclerosis

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Two male rhesus monkeys underwent cyclical feeding of a hypercholesterolemlc diet (2% cholesterol, 25% coconut oil) and a low-fat Purina monkey chow diet. During the latter diet, high density lipoprotein (HDL) exhibited two components with peak densities of d = 1.081 g/ml and 1.109 g/ml named HDL L and HDLH, respectively. During the Initial hypercholesterolemic stage, except for apo A-ll which remained unchanged, there was a transient rise In HDL (mainly HDLJ as well as in HDL cholesterol and apo A-l, all reaching maximal values after about 2 weeks from the onset of the diet. The two HDL species changed neither In size nor density as compared to their baseline counterparts, but had a comparatively higher content In cholesteryl ester and lesser amounts of triglycerides and phospholipids as compared to the normocholesterolemic animal. With the development of overt hypercholesterolemia (plasma cholesterol levels above 400 mg/dl), both HDL particles increased in density due to the loss of surface components (phospholipids and unesterlfled cholesterol) and core triglycerides with only minor changes in protein and cholesteryl ester contents. At this stage, the same two animals exhibited significant changes in the size and buoyant density of LDL. When returned to a normal Purina chow diet, the animals' serum cholesterol levels declined rapidly to normal levels; normalization of the HDL distribution also occurred but at a comparatively later time (26 weeks).Our studies Indicate that the two HDL subsets characteristic of the normocholesterolemic rhesus monkey undergo significant changes in buoyant density as a function of the stage of hypercholesterolemia and that changes In concentration and size mainly affect the HDL L subspecies. At levels of plasma cholesterol below 400 mg/dl, this cholesterol Increment Is reflected by a significant increase in the number of the HDL subspecies without the overt participation of the low density lipoprotein classes characteristic of the advanced hyperlipldemlc stage. Since we previously reported that greatly increased levels of cholesteryl esters enriched low density lipoproteins, (J-VLDL (very low density lipoprotein) and pre-B-VLDL during overt diet-Induced hypercholesterolemia, it is apparent that cholesterol is distributed differently among lipoprotein particles containing either apo A-l, apo B, or apo E depending on its concentration In plasma. (Arteriosclerosis 4:154-164, March/April 1984) R hesus monkeys fed high cholesterol diets develop altered concentrations of plasma lipoproteins. Since there may be a causal relationship between the level of serum low density lipoprotein (LDL) and atherosclerosis, most attention has been focused on LDL. However, the concentration and Received July 7,1983; revision accepted November 18, 1983. density distribution of HDL species are also affected by cholesterol-containing diets. Thus, it was observed that high density lipoprotein (HDL) levels were temporarily increased in rhesus and sooty mangabey monkeys on a high cholesterol diet but fell...

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“…5 Blood was collected frorti the femoral vein of monkeys anesthetized with ketamine and the serum was separated by centrifuging the blood at 4°C for 30 minutes at 1000 g.…”

Section: Methodsmentioning

confidence: 99%

Section: Chemical Analysismentioning

confidence: 99%

See 1 more Smart Citation

Response of rhesus serum high density lipoproteins to cycles of diet-induced hypercholesterolemia.

Fless¹,

Juhn²,

Karlin³

et al. 1984

Arteriosclerosis

Self Cite

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“…Lp(a) was first recognized in rhesus monkeys by Fless et al 13 Later, Nevan et al 14 reported a relation between plasma Lp(a) levels, apolipoprotein (a) (apo[a]) isoforms, and low density lipoprotein receptor function. Azrolan et al 15 reported that Lp(a) from cynomolgus monkeys is immunochemically and quantitatively similar to human Lp(a).…”

Section: Studies On Plasma Lp(a) In Macaquesmentioning

confidence: 99%

Occlusive arterial thrombosis in cynomolgus monkeys with varying plasma concentrations of lipoprotein(a).

Williams

Bellinger

Nichols

et al. 1993

Arterioscler Thromb

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Lipoprotein(a) (Lp[a]) is a newly recognized risk factor for the development of coronary heart disease and stroke in human beings; however, the mechanisms by which Lp(a) increases the risk of coronary heart disease remain unclear. The purpose of this study was to examine the effects of Lp(a) on the occurrence of occlusive arterial thrombosis. Occlusive arterial thrombus formation was examined in 18 cynomolgus monkeys with high plasma Lp(a) concentrations (> 35 mg/dL, n = 6), intermediate Lp(a) concentrations (20-25 mg/dL, n = 6), and low Lp(a) concentrations (< 12 mg/dL, n = 6). A Goldblatt clamp was positioned around the left common carotid artery to produce a stenotic segment, and the artery was pinch-injured with needle holders. A 20-MHz Doppler velocity crystal, placed distal to the stenosis/injury site, was used to detect cyclic flow reductions (indicative of transient thrombosis) or permanent cessation of flow velocity (indicative of more stable occlusive thrombosis). All monkeys with high Lp(a) concentrations developed permanent cessation of flow, whereas only one of six arteries from low-Lp(a) monkeys developed permanent cessation of flow (p < 0.05). Arteries from monkeys with intermediate Lp(a) concentrations developed pronounced cyclic reductions of flow but did not progress to permanent cessation of flow. There were no differences in plasma von Willebrand factor activity among the three groups. Immunohistochemical analysis of the damaged arterial segments indicated incorporation of Lp(a) into the adventitia, media, and intima of arteries from monkeys with low and high plasma Lp(a) concentrations, as well as the presence of an occlusive thrombus in arteries that developed permanent cessation of flow.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…The wisdom of this advice is questionable because several studies (22)(23)(24) show coconut oil, which is rich in caproic (8 : 0) and caprylic (10 : 0) acid as well as lauric (12 : 0) and myristic (12 : 0) acids, raises LDL-C and the TC: HDL-C ratio compared with olive oil or palm olein where the SFA are provided mainly by palmitic acid. Furthermore, coconut oil is relatively atherogenic in animal models especially when fed with dietary cholesterol (25) . In contrast, palm oil, which is rich in palmitic acid, does not have different effects on LDL-C from high oleic acid safflower oil in primates in the absence of dietary cholesterol (26) .…”

Section: Effects Of Different Sfa On Serum Lipids and Lipoproteinsmentioning

confidence: 99%

Reappraisal of SFA and cardiovascular risk

Sanders

2013

Proc. Nutr. Soc.

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This review reappraises dietary advice to reduce and replace SFA for the prevention of CVD. In the 1970s, SFA accounted for about 18% UK food energy, by 2001 it had fallen to 13% and continues to be above the <11% target. Compared with carbohydrates, C 12 -C 16 SFA raise serum total cholesterol (TC), LDL-cholesterol (LDL-C) and HDL-cholesterol (HDL-C) without affecting the TC:HDL-C ratio; other SFA have neutral effects on the fasting lipid profile. Replacing 3% dietary SFA with MUFA or PUFA lowers LDL-C by 2% and TC:HDL-C ratio by 0·03. No other specific adverse effects of SFA compared with MUFA on risk CVD factors have been proven. Meta-analyses of prospective cohort studies report the relative risks (95% CI) of high v. low intakes of SFA to be 1·07 (0·96, 1·19) for CHD, 0·81 (0·62, 1·05) for stroke and 1·00 (0·89, 1·11) for CVD mortality and were not statistically significant. Exchanging 5% energy SFA for PUFA or carbohydrates found hazard ratios (95% CI) for CHD death to be 26% (−23, −3) and 4% (−18, 12; NS) lower, respectively. Meta-analysis of randomised controlled trials with clinical endpoints reports mean reductions (95% CI) of 14% (4, 23) in CHD incidence and 6% (−25, 4; NS) in mortality in trials, where SFA was lowered by decreasing and/or modifying dietary fat. In conclusion, SFA intakes are now close to guideline amounts and further reductions may only have a minor impact on CVD.

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Structural and functional changes of rhesus serum low density lipoproteins during cycles of diet-induced hypercholesterolemia.

Cited by 40 publications

References 25 publications

Response of rhesus serum high density lipoproteins to cycles of diet-induced hypercholesterolemia.

Response of rhesus serum high density lipoproteins to cycles of diet-induced hypercholesterolemia.

Occlusive arterial thrombosis in cynomolgus monkeys with varying plasma concentrations of lipoprotein(a).

Reappraisal of SFA and cardiovascular risk

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